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Why do some mammals have incomplete orbits?

Why do some mammals have incomplete orbits?


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I've noticed that a lot of carnivorous/omnivorous mammals (most, if not all the members of carnivora and some ancestral cetaceans), as well as some herbivores (marsupials), have incomplete orbits that merge into the temple near the zygomatic arch. I'm wondering what the evolutionary purpose of this is, as well as why we would lack them.


Incomplete Dominance

Incomplete dominance is when a dominant allele, or form of a gene, does not completely mask the effects of a recessive allele, and the organism’s resulting physical appearance shows a blending of both alleles. It is also called semi-dominance or partial dominance. One example is shown in roses. The allele for red color is dominant over the allele for white color, but heterozygous roses, which have both alleles, are pink. Note that this is different from codominance, which is when both alleles are expressed at the same time.


Single and Double Circulatory Systems

  • The animal transport system consists of:
    • A fluid medium to transport substances (the Blood)
    • A pump to push the fluid around the body
    • Specialised exchange surfaces

    Most transport systems also contain tubes (Blood Vessels) to hold the blood.

    This is the Circulatory System, which is a very efficient transport system.

    • A Single Circulatory System is a simple loop in which blood flows: Heart > Gills > Body > Heart
    • A Double Circulatory System is a double loop in which blood flows: Heart > Lungs > Heart > Body > Heart

    Fish have a single circulatory system, while mammals have a double circulatory system.

    In a double circulatory system, the loop that goes to the lungs is called the Pulmonary Circuit, while the loop that goes to the body is called the Systemic Circuit.

    The double circulatory system is advantageous for active animals since, while in the single circulatory system the blood pressure is limited by the delicate nature of the tiny capillaries in the gills, in the double circulatory system the blood pressure can be high in the systemic circuit while remaining low and safe in the pulmonary circuit. This allows animals with a double circulatory system to be more active, since blood can reach their respiring tissues faster due to the higher pressure.

    Fish are not as active as other animals, so their single circulatory system is sufficient for their needs, while more active animals like mammals need a double circulatory system.


    Contents

    Cycle of X-chromosome activation in rodents Edit

    The paragraphs below have to do only with rodents and do not reflect XI in the majority of mammals. X-inactivation is part of the activation cycle of the X chromosome throughout the female life. The egg and the fertilized zygote initially use maternal transcripts, and the whole embryonic genome is silenced until zygotic genome activation. Thereafter, all mouse cells undergo an early, imprinted inactivation of the paternally-derived X chromosome in 4–8 cell stage embryos. [3] [4] [5] [6] The extraembryonic tissues (which give rise to the placenta and other tissues supporting the embryo) retain this early imprinted inactivation, and thus only the maternal X chromosome is active in these tissues.

    In the early blastocyst, this initial, imprinted X-inactivation is reversed in the cells of the inner cell mass (which give rise to the embryo), and in these cells both X chromosomes become active again. Each of these cells then independently and randomly inactivates one copy of the X chromosome. [5] This inactivation event is irreversible during the lifetime of the individual, with the exception of the germline. In the female germline before meiotic entry, X-inactivation is reversed, so that after meiosis all haploid oocytes contain a single active X chromosome.

    Overview Edit

    The Xi marks the inactive, Xa the active X chromosome. X P denotes the paternal, and X M to denotes the maternal X chromosome. When the egg (carrying X M ), is fertilized by a sperm (carrying a Y or an X P ) a diploid zygote forms. From zygote, through adult stage, to the next generation of eggs, the X chromosome undergoes the following changes:

    1. Xi P Xi M zygote → undergoing zygotic genome activation, leading to:
    2. Xa PXa M → undergoing imprinted (paternal) X-inactivation, leading to:
    3. Xi P Xa M → undergoing X-activation in the early blastocyst stage, leading to:
    4. Xa P Xa M → undergoing random X-inactivation in the embryonic lineage (inner cell mass) in the blastocyst stage, leading to:
    5. Xi P Xa M OR Xa P Xi M → undergoing X-reactivation in primordial germ cells before meiosis, leading to:
    6. Xa MXa P diploid germ cells in meiotic arrest. As the meiosis I only completes with ovulation, human germ cells exist in this stage from the first weeks of development until puberty. The completion of meiosis leads to:
    7. Xa M AND Xa P haploid germ cells (eggs).

    The X activation cycle has been best studied in mice, but there are multiple studies in humans. As most of the evidence is coming from mice, the above scheme represents the events in mice. The completion of the meiosis is simplified here for clarity. Steps 1–4 can be studied in in vitro fertilized embryos, and in differentiating stem cells X-reactivation happens in the developing embryo, and subsequent (6–7) steps inside the female body, therefore much harder to study.

    Timing Edit

    The timing of each process depends on the species, and in many cases the precise time is actively debated. [The whole part of the human timing of X-inactivation in this table is highly questionable and should be removed until properly substantiated by empirical data]

    Approximate timing of major events in the X chromosome activation cycle
    Process Mouse Human
    1 Zygotic genome activation 2–4 cell stage [7] 2–8 cell stage [7]
    2 Imprinted (paternal) X-inactivation 4–8 cell stage [6] [8] Unclear if it takes place in humans [9]
    3 X-activation Early blastocyst stage Early blastocyst stage
    4 Random X-inactivation in the embryonic lineage (inner cell mass) Late blastocyst stage Late blastocyst stage, after implantation [9]
    5 X-reactivation in primordial germ cells before meiosis From before developmental week 4 up to week 14 [10] [11]

    Inheritance of inactivation status across cell generations Edit

    The descendants of each cell which inactivated a particular X chromosome will also inactivate that same chromosome. This phenomenon, which can be observed in the coloration of tortoiseshell cats when females are heterozygous for the X-linked gene, should not be confused with mosaicism, which is a term that specifically refers to differences in the genotype of various cell populations in the same individual X-inactivation, which is an epigenetic change that results in a different phenotype, is not a change at the genotypic level. For an individual cell or lineage the inactivation is therefore skewed or 'non-random', and this can give rise to mild symptoms in female 'carriers' of X-linked genetic disorders. [12]

    Selection of one active X chromosome Edit

    Normal females possess two X chromosomes, and in any given cell one chromosome will be active (designated as Xa) and one will be inactive (Xi). However, studies of individuals with extra copies of the X chromosome show that in cells with more than two X chromosomes there is still only one Xa, and all the remaining X chromosomes are inactivated. This indicates that the default state of the X chromosome in females is inactivation, but one X chromosome is always selected to remain active.

    It is understood that X-chromosome inactivation is a random process, occurring at about the time of gastrulation in the epiblast (cells that will give rise to the embryo). The maternal and paternal X chromosomes have an equal probability of inactivation. This would suggest that women would be expected to suffer from X-linked disorders approximately 50% as often as men (because women have two X chromosomes, while men have only one) however, in actuality, the occurrence of these disorders in females is much lower than that. One explanation for this disparity is that 12–20% [13] of genes on the inactivated X chromosome remain expressed, thus providing women with added protection against defective genes coded by the X-chromosome. Some [ who? ] suggest that this disparity must be evidence of preferential (non-random) inactivation. Preferential inactivation of the paternal X-chromosome occurs in both marsupials and in cell lineages that form the membranes surrounding the embryo, [14] whereas in placental mammals either the maternally or the paternally derived X-chromosome may be inactivated in different cell lines. [15]

    The time period for X-chromosome inactivation explains this disparity. Inactivation occurs in the epiblast during gastrulation, which gives rise to the embryo. [16] Inactivation occurs on a cellular level, resulting in a mosaic expression, in which patches of cells have an inactive maternal X-chromosome, while other patches have an inactive paternal X-chromosome. For example, a female heterozygous for haemophilia (an X-linked disease) would have about half of her liver cells functioning properly, which is typically enough to ensure normal blood clotting. [17] [18] Chance could result in significantly more dysfunctional cells however, such statistical extremes are unlikely. Genetic differences on the chromosome may also render one X-chromosome more likely to undergo inactivation. Also, if one X-chromosome has a mutation hindering its growth or rendering it non viable, cells which randomly inactivated that X will have a selective advantage over cells which randomly inactivated the normal allele. Thus, although inactivation is initially random, cells that inactivate a normal allele (leaving the mutated allele active) will eventually be overgrown and replaced by functionally normal cells in which nearly all have the same X-chromosome activated. [17]

    It is hypothesized [ by whom? ] that there is an autosomally-encoded 'blocking factor' which binds to the X chromosome and prevents its inactivation. The model postulates that there is a limiting blocking factor, so once the available blocking factor molecule binds to one X chromosome the remaining X chromosome(s) are not protected from inactivation. This model is supported by the existence of a single Xa in cells with many X chromosomes and by the existence of two active X chromosomes in cell lines with twice the normal number of autosomes. [19]

    Sequences at the X inactivation center (XIC), present on the X chromosome, control the silencing of the X chromosome. The hypothetical blocking factor is predicted to bind to sequences within the XIC.

    Expression of X-linked disorders in heterozygous females Edit

    The effect of female X heterozygosity is apparent in some localized traits, such as the unique coat pattern of a calico cat. It can be more difficult, however, to fully understand the expression of un-localized traits in these females, such as the expression of disease.

    Since males only have one copy of the X chromosome, all expressed X-chromosomal genes (or alleles, in the case of multiple variant forms for a given gene in the population) are located on that copy of the chromosome. Females, however, will primarily express the genes or alleles located on the X-chromosomal copy that remains active. Considering the situation for one gene or multiple genes causing individual differences in a particular phenotype (i.e., causing variation observed in the population for that phenotype), in homozygous females it doesn't particularly matter which copy of the chromosome is inactivated, as the alleles on both copies are the same. However, in females that are heterozygous at the causal genes, the inactivation of one copy of the chromosome over the other can have a direct impact on their phenotypic value. Because of this phenomenon, there is an observed increase in phenotypic variation in females that are heterozygous at the involved gene or genes than in females that are homozygous at that gene or those genes. [20] There are many different ways in which the phenotypic variation can play out. In many cases, heterozygous females may be asymptomatic or only present minor symptoms of a given disorder, such as with X-linked adrenoleukodystrophy. [21]

    The differentiation of phenotype in heterozygous females is furthered by the presence of X-inactivation skewing. Typically, each X-chromosome is silenced in half of the cells, but this process is skewed when preferential inactivation of a chromosome occurs. It is thought that skewing happens either by chance or by a physical characteristic of a chromosome that may cause it to be silenced more or less often, such as an unfavorable mutation. [22] [23]

    On average, each X chromosome is inactivated in half of the cells, however 5-20% of "apparently normal" women display X-inactivation skewing. [22] In cases where skewing is present, a broad range of symptom expression can occur, resulting in expression varying from minor to severe depending on the skewing proportion. An extreme case of this was seen where monozygotic female twins had extreme variance in expression of Menkes disease (an X-linked disorder) resulting in the death of one twin while the other remained asymptomatic. [24]

    It is thought that X-inactivation skewing could be caused by issues in the mechanism that causes inactivation, or by issues in the chromosome itself. [22] [23] However, the link between phenotype and skewing is still being questioned, and should be examined on a case-by-case basis. A study looking at both symptomatic and asymptomatic females who were heterozygous for Duchenne and Becker muscular dystrophies (DMD) found no apparent link between transcript expression and skewed X-Inactivation. The study suggests that both mechanisms are independently regulated, and there are other unknown factors at play. [25]

    Chromosomal component Edit

    The X-inactivation center (or simply XIC) on the X chromosome is necessary and sufficient to cause X-inactivation. Chromosomal translocations which place the XIC on an autosome lead to inactivation of the autosome, and X chromosomes lacking the XIC are not inactivated. [26] [27]

    The XIC contains four non-translated RNA genes, Xist, Tsix, Jpx and Ftx, which are involved in X-inactivation. The XIC also contains binding sites for both known and unknown regulatory proteins. [28]

    Xist and Tsix RNAs Edit

    The X-inactive specific transcript (Xist) gene encodes a large non-coding RNA that is responsible for mediating the specific silencing of the X chromosome from which it is transcribed. [29] The inactive X chromosome is coated by Xist RNA, [30] whereas the Xa is not (See Figure to the right). X chromosomes that lack the Xist gene cannot be inactivated. [31] Artificially placing and expressing the Xist gene on another chromosome leads to silencing of that chromosome. [32] [26]

    Prior to inactivation, both X chromosomes weakly express Xist RNA from the Xist gene. During the inactivation process, the future Xa ceases to express Xist, whereas the future Xi dramatically increases Xist RNA production. On the future Xi, the Xist RNA progressively coats the chromosome, spreading out from the XIC [32] the Xist RNA does not localize to the Xa. The silencing of genes along the Xi occurs soon after coating by Xist RNA.

    Like Xist, the Tsix gene encodes a large RNA which is not believed to encode a protein. The Tsix RNA is transcribed antisense to Xist, meaning that the Tsix gene overlaps the Xist gene and is transcribed on the opposite strand of DNA from the Xist gene. [27] Tsix is a negative regulator of Xist X chromosomes lacking Tsix expression (and thus having high levels of Xist transcription) are inactivated much more frequently than normal chromosomes.

    Like Xist, prior to inactivation, both X chromosomes weakly express Tsix RNA from the Tsix gene. Upon the onset of X-inactivation, the future Xi ceases to express Tsix RNA (and increases Xist expression), whereas Xa continues to express Tsix for several days.

    Rep A is a long non coding RNA that works with another long non coding RNA, Xist, for X inactivation. Rep A inhibits the function of Tsix, the antisense of Xist, in conjunction with eliminating expression of Xite. It promotes methylation of the Tsix region by attracting PRC2 and thus inactivating one of the X chromosomes. [28]

    Silencing Edit

    The inactive X chromosome does not express the majority of its genes, unlike the active X chromosome. This is due to the silencing of the Xi by repressive heterochromatin, which compacts the Xi DNA and prevents the expression of most genes.

    Compared to the Xa, the Xi has high levels of DNA methylation, low levels of histone acetylation, low levels of histone H3 lysine-4 methylation, and high levels of histone H3 lysine-9 methylation and H3 lysine-27 methylation mark which is placed by the PRC2 complex recruited by Xist, all of which are associated with gene silencing. [33] PRC2 regulates chromatin compaction and chromatin remodeling in several processes including the DNA damage response. [34] Additionally, a histone variant called macroH2A (H2AFY) is exclusively found on nucleosomes along the Xi. [35] [36]

    Barr bodies Edit

    DNA packaged in heterochromatin, such as the Xi, is more condensed than DNA packaged in euchromatin, such as the Xa. The inactive X forms a discrete body within the nucleus called a Barr body. [37] The Barr body is generally located on the periphery of the nucleus, is late replicating within the cell cycle, and, as it contains the Xi, contains heterochromatin modifications and the Xist RNA.

    Expressed genes on the inactive X chromosome Edit

    A fraction of the genes along the X chromosome escape inactivation on the Xi. The Xist gene is expressed at high levels on the Xi and is not expressed on the Xa. [38] Many other genes escape inactivation some are expressed equally from the Xa and Xi, and others, while expressed from both chromosomes, are still predominantly expressed from the Xa. [39] [40] [41] Up to one quarter of genes on the human Xi are capable of escape. [39] Studies in the mouse suggest that in any given cell type, 3% to 15% of genes escape inactivation, and that escaping gene identity varies between tissues. [40] [41]

    Many of the genes which escape inactivation are present along regions of the X chromosome which, unlike the majority of the X chromosome, contain genes also present on the Y chromosome. These regions are termed pseudoautosomal regions, as individuals of either sex will receive two copies of every gene in these regions (like an autosome), unlike the majority of genes along the sex chromosomes. Since individuals of either sex will receive two copies of every gene in a pseudoautosomal region, no dosage compensation is needed for females, so it is postulated that these regions of DNA have evolved mechanisms to escape X-inactivation. The genes of pseudoautosomal regions of the Xi do not have the typical modifications of the Xi and have little Xist RNA bound.

    The existence of genes along the inactive X which are not silenced explains the defects in humans with abnormal numbers of the X chromosome, such as Turner syndrome (X0) or Klinefelter syndrome (XXY). Theoretically, X-inactivation should eliminate the differences in gene dosage between affected individuals and individuals with a normal chromosome complement. In affected individuals, however, X-inactivation is incomplete and the dosage of these non-silenced genes will differ as they escape X-inactivation, similar to an autosomal aneuploidy.

    The precise mechanisms that control escape from X-inactivation are not known, but silenced and escape regions have been shown to have distinct chromatin marks. [40] [42] It has been suggested that escape from X-inactivation might be mediated by expression of long non-coding RNA (lncRNA) within the escaping chromosomal domains. [2]

    Stanley Michael Gartler used X-chromosome inactivation to demonstrate the clonal origin of cancers. Examining normal tissues and tumors from females heterozygous for isoenzymes of the sex-linked G6PD gene demonstrated that tumor cells from such individuals express only one form of G6PD, whereas normal tissues are composed of a nearly equal mixture of cells expressing the two different phenotypes. This pattern suggests that a single cell, and not a population, grows into a cancer. [43] However, this pattern has been proven wrong for many cancer types, suggesting that some cancers may be polyclonal in origin. [44]

    Besides, measuring the methylation (inactivation) status of the polymorphic human androgen receptor (HUMARA) located on X-chromosome is considered the most accurate method to assess clonality in female cancer biopsies. [45] A great variety of tumors was tested by this method, some, such as renal cell carcinoma, [46] found monoclonal while others (e.g. mesothelioma [47] ) were reported polyclonal.

    Researchers have also investigated using X-chromosome inactivation to silence the activity of autosomal chromosomes. For example, Jiang et al. inserted a copy of the Xist gene into one copy of chromosome 21 in stem cells derived from an individual with trisomy 21 (Down syndrome). [48] The inserted Xist gene induces Barr body formation, triggers stable heterochromatin modifications, and silences most of the genes on the extra copy of chromosome 21. In these modified stem cells, the Xist-mediated gene silencing seems to reverse some of the defects associated with Down syndrome.

    In 1959 Susumu Ohno showed that the two X chromosomes of mammals were different: one appeared similar to the autosomes the other was condensed and heterochromatic. [49] This finding suggested, independently to two groups of investigators, that one of the X chromosomes underwent inactivation.

    In 1961, Mary Lyon proposed the random inactivation of one female X chromosome to explain the mottled phenotype of female mice heterozygous for coat color genes. [50] The Lyon hypothesis also accounted for the findings that one copy of the X chromosome in female cells was highly condensed, and that mice with only one copy of the X chromosome developed as infertile females. This suggested [51] to Ernest Beutler, studying heterozygous females for glucose-6-phosphate dehydrogenase (G6PD) deficiency, that there were two red cell populations of erythrocytes in such heterozygotes: deficient cells and normal cells, [52] depending on whether the inactivated X chromosome (in the nucleus of the red cell's precursor cell) contains the normal or defective G6PD allele.


    Contents

    Some species reproduce exclusively by parthenogenesis (such as the bdelloid rotifers), while others can switch between sexual reproduction and parthenogenesis. This is called facultative parthenogenesis (other terms are cyclical parthenogenesis, heterogamy [9] [10] or heterogony [11] [12] ). The switch between sexuality and parthenogenesis in such species may be triggered by the season (aphid, some gall wasps), or by a lack of males or by conditions that favour rapid population growth (rotifers and cladocerans like Daphnia). In these species asexual reproduction occurs either in summer (aphids) or as long as conditions are favourable. This is because in asexual reproduction a successful genotype can spread quickly without being modified by sex or wasting resources on male offspring who won't give birth. In times of stress, offspring produced by sexual reproduction may be fitter as they have new, possibly beneficial gene combinations. In addition, sexual reproduction provides the benefit of meiotic recombination between non-sister chromosomes, a process associated with repair of DNA double-strand breaks and other DNA damages that may be induced by stressful conditions. [13]

    Many taxa with heterogony have within them species that have lost the sexual phase and are now completely asexual. Many other cases of obligate parthenogenesis (or gynogenesis) are found among polyploids and hybrids where the chromosomes cannot pair for meiosis.

    The production of female offspring by parthenogenesis is referred to as thelytoky (e.g., aphids) while the production of males by parthenogenesis is referred to as arrhenotoky (e.g., bees). When unfertilized eggs develop into both males and females, the phenomenon is called deuterotoky. [14]

    Parthenogenesis can occur without meiosis through mitotic oogenesis. This is called apomictic parthenogenesis. Mature egg cells are produced by mitotic divisions, and these cells directly develop into embryos. In flowering plants, cells of the gametophyte can undergo this process. The offspring produced by apomictic parthenogenesis are full clones of their mother. Examples include aphids.

    Parthenogenesis involving meiosis is more complicated. In some cases, the offspring are haploid (e.g., male ants). In other cases, collectively called automictic parthenogenesis, the ploidy is restored to diploidy by various means. This is because haploid individuals are not viable in most species. In automictic parthenogenesis, the offspring differ from one another and from their mother. They are called half clones of their mother.

    Automictic Edit

    Automixis [15] is a term that covers several reproductive mechanisms, some of which are parthenogenetic. [16]

    Diploidy might be restored by the doubling of the chromosomes without cell division before meiosis begins or after meiosis is completed. This is referred to as an endomitotic cycle. This may also happen by the fusion of the first two blastomeres. Other species restore their ploidy by the fusion of the meiotic products. The chromosomes may not separate at one of the two anaphases (called restitutional meiosis) or the nuclei produced may fuse or one of the polar bodies may fuse with the egg cell at some stage during its maturation.

    Some authors consider all forms of automixis sexual as they involve recombination. Many others classify the endomitotic variants as asexual and consider the resulting embryos parthenogenetic. Among these authors, the threshold for classifying automixis as a sexual process depends on when the products of anaphase I or of anaphase II are joined together. The criterion for "sexuality" varies from all cases of restitutional meiosis, [17] to those where the nuclei fuse or to only those where gametes are mature at the time of fusion. [16] Those cases of automixis that are classified as sexual reproduction are compared to self-fertilization in their mechanism and consequences.

    The genetic composition of the offspring depends on what type of apomixis takes place. When endomitosis occurs before meiosis [18] [19] or when central fusion occurs (restitutional meiosis of anaphase I or the fusion of its products), the offspring get all [18] [20] to more than half of the mother's genetic material and heterozygosity is mostly preserved [21] (if the mother has two alleles for a locus, it is likely that the offspring will get both). This is because in anaphase I the homologous chromosomes are separated. Heterozygosity is not completely preserved when crossing over occurs in central fusion. [22] In the case of pre-meiotic doubling, recombination -if it happens- occurs between identical sister chromatids. [18]

    If terminal fusion (restitutional meiosis of anaphase II or the fusion of its products) occurs, a little over half the mother's genetic material is present in the offspring and the offspring are mostly homozygous. [23] This is because at anaphase II the sister chromatids are separated and whatever heterozygosity is present is due to crossing over. In the case of endomitosis after meiosis, the offspring is completely homozygous and has only half the mother's genetic material.

    This can result in parthenogenetic offspring being unique from each other and from their mother.

    Sex of the offspring Edit

    In apomictic parthenogenesis, the offspring are clones of the mother and hence (except for aphids) are usually female. In the case of aphids, parthenogenetically produced males and females are clones of their mother except that the males lack one of the X chromosomes (XO). [24]

    When meiosis is involved, the sex of the offspring will depend on the type of sex determination system and the type of apomixis. In species that use the XY sex-determination system, parthenogenetic offspring will have two X chromosomes and are female. In species that use the ZW sex-determination system the offspring genotype may be one of ZW (female), [20] [21] ZZ (male), or WW (non-viable in most species [23] but a fertile, [ dubious – discuss ] viable female in a few (e.g., boas)). [23] ZW offspring are produced by endoreplication before meiosis or by central fusion. [20] [21] ZZ and WW offspring occur either by terminal fusion [23] or by endomitosis in the egg cell.

    In polyploid obligate parthenogens like the whiptail lizard, all the offspring are female. [19]

    In many hymenopteran insects such as honeybees, female eggs are produced sexually, using sperm from a drone father, while the production of further drones (males) depends on the queen (and occasionally workers) producing unfertilized eggs. This means that females (workers and queens) are always diploid, while males (drones) are always haploid, and produced parthenogenetically.

    Facultative Edit

    Facultative parthenogenesis is the term for when a female can produce offspring either sexually or via asexual reproduction. [25] Facultative parthenogenesis is extremely rare in nature, with only a few examples of animal taxa capable of facultative parthenogenesis. [25] One of the best-known examples of taxa exhibiting facultative parthenogenesis are mayflies presumably, this is the default reproductive mode of all species in this insect order. [26] Facultative parthenogenesis is believed to be a response to a lack of a viable male. A female may undergo facultative parthenogenesis if a male is absent from the habitat or if it is unable to produce viable offspring.

    In aphids, a generation sexually conceived by a male and a female produces only females. The reason for this is the non-random segregation of the sex chromosomess X and O during spermatogenesis. [27]

    Facultative parthenogenesis is often used to describe cases of spontaneous parthenogenesis in normally sexual animals. [28] For example, many cases of spontaneous parthenogenesis in sharks, some snakes, Komodo dragons and a variety of domesticated birds were widely attributed to facultative parthenogenesis. [29] These cases are examples of spontaneous parthenogenesis. [25] [28] The occurrence of such asexually produced eggs in sexual animals can be explained by a meiotic error, leading to eggs produced via automixis. [28] [30]

    Obligate Edit

    Obligate parthenogenesis is the process in which organisms exclusively reproduce through asexual means. [31] Many species have been shown to transition to obligate parthenogenesis over evolutionary time. Well documented transitions to obligate parthenogenesis have been found in numerous metazoan taxa, albeit through highly diverse mechanisms. These transitions often occur as a result of inbreeding or mutation within large populations. [32] There are a number of documented species, specifically salamanders and geckos, that rely on obligate parthenogenesis as their major method of reproduction. As such, there are over 80 species of unisex reptiles (mostly lizards but including a single snake species), amphibians and fishes in nature for which males are no longer a part of the reproductive process. [33] A female will produce an ovum with a full set (two sets of genes) provided solely by the mother. Thus, a male is not needed to provide sperm to fertilize the egg. This form of asexual reproduction is thought in some cases to be a serious threat to biodiversity for the subsequent lack of gene variation and potentially decreased fitness of the offspring. [31]

    Some invertebrate species that feature (partial) sexual reproduction in their native range are found to reproduce solely by parthenogenesis in areas to which they have been introduced. [34] [35] Relying solely on parthenogenetic reproduction has several advantages for an invasive species: it obviates the need for individuals in a very sparse initial population to search for mates, and an exclusively female sex distribution allows a population to multiply and invade more rapidly, potentially up to twice as fast. Examples include several aphid species [34] and the willow sawfly, Nematus oligospilus, which is sexual in its native Holarctic habitat but parthenogenetic where it has been introduced into the Southern Hemisphere. [35]

    Parthenogenesis is seen to occur naturally in aphids, Daphnia, rotifers, nematodes and some other invertebrates, as well as in many plants. Among vertebrates, strict parthenogenesis is only known to occur in lizards, snakes, [36] birds [37] and sharks, [38] with fish, amphibians and reptiles exhibiting various forms of gynogenesis and hybridogenesis (an incomplete form of parthenogenesis). [39] The first all-female (unisexual) reproduction in vertebrates was described in the fish Poecilia formosa in 1932. [40] Since then at least 50 species of unisexual vertebrate have been described, including at least 20 fish, 25 lizards, a single snake species, frogs, and salamanders. [39] Other usually sexual species may occasionally reproduce parthenogenetically the Komodo dragon and hammerhead and blacktip sharks are recent additions to the known list of spontaneous parthenogenetic vertebrates. As with all types of asexual reproduction, there are both costs (low genetic diversity and therefore susceptibility to adverse mutations that might occur) and benefits (reproduction without the need for a male) associated with parthenogenesis.

    Parthenogenesis is distinct from artificial animal cloning, a process where the new organism is necessarily genetically identical to the cell donor. In cloning, the nucleus of a diploid cell from a donor organism is inserted into an enucleated egg cell and the cell is then stimulated to undergo continued mitosis, resulting in an organism that is genetically identical to the donor. Parthenogenesis is different, in that it originates from the genetic material contained within an egg cell and the new organism is not necessarily genetically identical to the parent.

    Parthenogenesis may be achieved through an artificial process as described below under the discussion of mammals.

    Oomycetes Edit

    Apomixis can apparently occur in Phytophthora, [41] an oomycete. Oospores from an experimental cross were germinated, and some of the progeny were genetically identical to one or other parent, implying that meiosis did not occur and the oospores developed by parthenogenesis.

    Velvet worms Edit

    No males of Epiperipatus imthurni have been found, and specimens from Trinidad were shown to reproduce parthenogenetically. This species is the only known velvet worm to reproduce via parthenogenesis. [42]

    Rotifers Edit

    In bdelloid rotifers, females reproduce exclusively by parthenogenesis (obligate parthenogenesis), [43] while in monogonont rotifers, females can alternate between sexual and asexual reproduction (cyclical parthenogenesis). At least in one normally cyclical parthenogenetic species obligate parthenogenesis can be inherited: a recessive allele leads to loss of sexual reproduction in homozygous offspring. [44]

    Flatworms Edit

    At least two species in the genus Dugesia, flatworms in the Turbellaria sub-division of the phylum Platyhelminthes, include polyploid individuals that reproduce by parthenogenesis. [45] This type of parthenogenesis requires mating, but the sperm does not contribute to the genetics of the offspring (the parthenogenesis is pseudogamous, alternatively referred to as gynogenetic). A complex cycle of matings between diploid sexual and polyploid parthenogenetic individuals produces new parthenogenetic lines.

    Snails Edit

    Several species of parthenogenetic gastropods have been studied, especially with respect to their status as invasive species. Such species include the New Zealand mud snail (Potamopyrgus antipodarum), [46] the red-rimmed melania (Melanoides tuberculata), [47] and the Quilted melania (Tarebia granifera). [48]

    Insects Edit

    Parthenogenesis in insects can cover a wide range of mechanisms. [49] The offspring produced by parthenogenesis may be of both sexes, only female (thelytoky, e.g. aphids and some hymenopterans [50] ) or only male (arrhenotoky, e.g. most hymenopterans). Both true parthenogenesis and pseudogamy (gynogenesis or sperm-dependent parthenogenesis) are known to occur. [25] The egg cells, depending on the species may be produced without meiosis (apomictically) or by one of the several automictic mechanisms.

    A related phenomenon, polyembryony is a process that produces multiple clonal offspring from a single egg cell. This is known in some hymenopteran parasitoids and in Strepsiptera. [49]

    In automictic species the offspring can be haploid or diploid. Diploids are produced by doubling or fusion of gametes after meiosis. Fusion is seen in the Phasmatodea, Hemiptera (Aleurodids and Coccidae), Diptera, and some Hymenoptera. [49]

    In addition to these forms is hermaphroditism, where both the eggs and sperm are produced by the same individual, but is not a type of parthenogenesis. This is seen in three species of Icerya scale insects. [49]

    Parasitic bacteria like Wolbachia have been noted to induce automictic thelytoky in many insect species with haplodiploid systems. They also cause gamete duplication in unfertilized eggs causing them to develop into female offspring. [49]

    Among species with the haplo-diploid sex-determination system, such as hymenopterans (ants, bees and wasps) and thysanopterans (thrips), haploid males are produced from unfertilized eggs. Usually, eggs are laid only by the queen, but the unmated workers may also lay haploid, male eggs either regularly (e.g. stingless bees) or under special circumstances. An example of non-viable parthenogenesis is common among domesticated honey bees. The queen bee is the only fertile female in the hive if she dies without the possibility of a viable replacement queen, it is not uncommon for the worker bees to lay eggs. This is a result of the lack of the queen's pheromones and the pheromones secreted by uncapped brood, which normally suppress ovarian development in workers. Worker bees are unable to mate, and the unfertilized eggs produce only drones (males), which can mate only with a queen. Thus, in a relatively short period, all the worker bees die off, and the new drones follow if they have not been able to mate before the collapse of the colony. This behavior is believed to have evolved to allow a doomed colony to produce drones which may mate with a virgin queen and thus preserve the colony's genetic progeny.

    A few ants and bees are capable of producing diploid female offspring parthenogenetically. These include a honey bee subspecies from South Africa, Apis mellifera capensis, where workers are capable of producing diploid eggs parthenogenetically, and replacing the queen if she dies other examples include some species of small carpenter bee, (genus Ceratina). Many parasitic wasps are known to be parthenogenetic, sometimes due to infections by Wolbachia.

    The workers in five [22] ant species and the queens in some ants are known to reproduce by parthenogenesis. In Cataglyphis cursor, a European formicine ant, the queens and workers can produce new queens by parthenogenesis. The workers are produced sexually. [22]

    In Central and South American electric ants, Wasmannia auropunctata, queens produce more queens through automictic parthenogenesis with central fusion. Sterile workers usually are produced from eggs fertilized by males. In some of the eggs fertilized by males, however, the fertilization can cause the female genetic material to be ablated from the zygote. In this way, males pass on only their genes to become fertile male offspring. This is the first recognized example of an animal species where both females and males can reproduce clonally resulting in a complete separation of male and female gene pools. [51] As a consequence, the males will only have fathers and the queens only mothers, while the sterile workers are the only ones with both parents of both genders.

    These ants get both the benefits of both asexual and sexual reproduction [22] [51] —the daughters who can reproduce (the queens) have all of the mother's genes, while the sterile workers whose physical strength and disease resistance are important are produced sexually.

    Other examples of insect parthenogenesis can be found in gall-forming aphids (e.g., Pemphigus betae), where females reproduce parthenogenetically during the gall-forming phase of their life cycle and in grass thrips. In the grass thrips genus Aptinothrips there have been, despite the very limited number of species in the genus, several transitions to asexuality. [52]

    Crustaceans Edit

    Crustacean reproduction varies both across and within species. The water flea Daphnia pulex alternates between sexual and parthenogenetic reproduction. [53] Among the better-known large decapod crustaceans, some crayfish reproduce by parthenogenesis. "Marmorkrebs" are parthenogenetic crayfish that were discovered in the pet trade in the 1990s. [54] Offspring are genetically identical to the parent, indicating it reproduces by apomixis, i.e. parthenogenesis in which the eggs did not undergo meiosis. [55] Spinycheek crayfish (Orconectes limosus) can reproduce both sexually and by parthenogenesis. [56] The Louisiana red swamp crayfish (Procambarus clarkii), which normally reproduces sexually, has also been suggested to reproduce by parthenogenesis, [57] although no individuals of this species have been reared this way in the lab. Artemia parthenogenetica is a species or series of populations of parthenogenetic brine shrimps. [58]

    Spiders Edit

    At least two species of spiders in the family Oonopidae (goblin spiders), Heteroonops spinimanus and Triaeris stenaspis, are thought to be parthenogenetic, as no males have ever been collected. Parthenogenetic reproduction has been demonstrated in the laboratory for T. stenaspis. [59]

    Sharks Edit

    Parthenogenesis in sharks has been confirmed in at least three species, the bonnethead, [38] the blacktip shark, [60] and the zebra shark, [61] and reported in others.

    A bonnethead, a type of small hammerhead shark, was found to have produced a pup, born live on December 14, 2001 at Henry Doorly Zoo in Nebraska, in a tank containing three female hammerheads, but no males. The pup was thought to have been conceived through parthenogenesis. The shark pup was apparently killed by a stingray within days of birth. [62] The investigation of the birth was conducted by the research team from Queen's University Belfast, Southeastern University in Florida, and Henry Doorly Zoo itself, and it was concluded after DNA testing that the reproduction was parthenogenetic. The testing showed the female pup's DNA matched only one female who lived in the tank, and that no male DNA was present in the pup. The pup was not a twin or clone of her mother, but rather, contained only half of her mother's DNA ("automictic parthenogenesis"). This type of reproduction had been seen before in bony fish, but never in cartilaginous fish such as sharks, until this documentation.

    In the same year, a female Atlantic blacktip shark in Virginia reproduced via parthenogenesis. [63] On October 10, 2008 scientists confirmed the second case of a "virgin birth" in a shark. The Journal of Fish Biology reported a study in which scientists said DNA testing proved that a pup carried by a female Atlantic blacktip shark in the Virginia Aquarium & Marine Science Center contained no genetic material from a male. [60]

    In 2002, two white-spotted bamboo sharks were born at the Belle Isle Aquarium in Detroit. They hatched 15 weeks after being laid. The births baffled experts as the mother shared an aquarium with only one other shark, which was female. The female bamboo sharks had laid eggs in the past. This is not unexpected, as many animals will lay eggs even if there is not a male to fertilize them. Normally, the eggs are assumed to be inviable and are discarded. This batch of eggs was left undisturbed by the curator as he had heard about the previous birth in 2001 in Nebraska and wanted to observe whether they would hatch. Other possibilities had been considered for the birth of the Detroit bamboo sharks including thoughts that the sharks had been fertilized by a male and stored the sperm for a period of time, as well as the possibility that the Belle Isle bamboo shark is a hermaphrodite, harboring both male and female sex organs, and capable of fertilizing its own eggs, but that is not confirmed. [64]

    In 2008, a Hungarian aquarium had another case of parthenogenesis after its lone female shark produced a pup without ever having come into contact with a male shark.

    The repercussions of parthenogenesis in sharks, which fails to increase the genetic diversity of the offspring, is a matter of concern for shark experts, taking into consideration conservation management strategies for this species, particularly in areas where there may be a shortage of males due to fishing or environmental pressures. Although parthenogenesis may help females who cannot find mates, it does reduce genetic diversity.

    In 2011, recurring shark parthenogenesis over several years was demonstrated in a captive zebra shark, a type of carpet shark. [61] [65] DNA genotyping demonstrated that individual zebra sharks can switch from sexual to parthenogenetic reproduction. [66]

    Amphibians Edit

    Squamata Edit

    Most reptiles of the squamatan order (lizards and snakes) reproduce sexually, but parthenogenesis has been observed to occur naturally in certain species of whiptails, some geckos, rock lizards, [5] [67] [68] Komodo dragons [69] and snakes. [70] Some of these like the mourning gecko Lepidodactylus lugubris, Indo-Pacific house gecko Hemidactylus garnotii, the hybrid whiptails Cnemidophorus, Caucasian rock lizards Darevskia, and the brahminy blindsnake, Indotyphlops braminus are unisexual and obligately parthenogenetic. Other reptiles, such as the Komodo dragon, other monitor lizards, [71] and some species of boas, [8] [23] [72] pythons, [21] [73] filesnakes, [74] [75] gartersnakes [76] and rattlesnakes [77] [78] were previously considered as cases of facultative parthenogenesis, but are in fact cases of accidental parthenogenesis. [28]

    In 2012, facultative parthenogenesis was reported in wild vertebrates for the first time by US researchers amongst captured pregnant copperhead and cottonmouth female pit-vipers. [79] The Komodo dragon, which normally reproduces sexually, has also been found able to reproduce asexually by parthenogenesis. [80] A case has been documented of a Komodo dragon reproducing via sexual reproduction after a known parthenogenetic event, [81] highlighting that these cases of parthenogenesis are reproductive accidents, rather than adaptive, facultative parthenogenesis. [28]

    Some reptile species use a ZW chromosome system, which produces either males (ZZ) or females (ZW). Until 2010, it was thought that the ZW chromosome system used by reptiles was incapable of producing viable WW offspring, but a (ZW) female boa constrictor was discovered to have produced viable female offspring with WW chromosomes. [82]

    Parthenogenesis has been studied extensively in the New Mexico whiptail in the genus Aspidoscelis of which 15 species reproduce exclusively by parthenogenesis. These lizards live in the dry and sometimes harsh climate of the southwestern United States and northern Mexico. All these asexual species appear to have arisen through the hybridization of two or three of the sexual species in the genus leading to polyploid individuals. The mechanism by which the mixing of chromosomes from two or three species can lead to parthenogenetic reproduction is unknown. Recently, a hybrid parthenogenetic whiptail lizard was bred in the laboratory from a cross between an asexual and a sexual whiptail. [83] Because multiple hybridization events can occur, individual parthenogenetic whiptail species can consist of multiple independent asexual lineages. Within lineages, there is very little genetic diversity, but different lineages may have quite different genotypes.

    An interesting aspect to reproduction in these asexual lizards is that mating behaviors are still seen, although the populations are all female. One female plays the role played by the male in closely related species, and mounts the female that is about to lay eggs. This behaviour is due to the hormonal cycles of the females, which cause them to behave like males shortly after laying eggs, when levels of progesterone are high, and to take the female role in mating before laying eggs, when estrogen dominates. Lizards who act out the courtship ritual have greater fecundity than those kept in isolation, due to the increase in hormones that accompanies the mounting. So, although the populations lack males, they still require sexual behavioral stimuli for maximum reproductive success. [84]

    Some lizard parthenogens show a pattern of geographic parthenogenesis, occupying high mountain areas where their ancestral forms have an inferior competition ability. [85] In Caucasian rock lizards of genus Darevskia, which have six parthenogenetic forms of hybrid origin [67] [68] [86] hybrid parthenogenetic form D. "dahli" has a broader niche than either of its bisexual ancestors and its expansion throughout the Central Lesser Caucasus caused decline of the ranges of both its maternal and paternal species. [87]

    Birds Edit

    Parthenogenesis in birds is known mainly from studies of domesticated turkeys and chickens, although it has also been noted in the domestic pigeon. [37] In most cases the egg fails to develop normally or completely to hatching. [37] [88] The first description of parthenogenetic development in a passerine was demonstrated in captive zebra finches, although the dividing cells exhibited irregular nuclei and the eggs did not hatch. [37]

    Parthenogenesis in turkeys appears to result from a conversion of haploid cells to diploid [88] most embryos produced in this way die early in development. Rarely, viable birds result from this process, and the rate at which this occurs in turkeys can be increased by selective breeding, [89] however male turkeys produced from parthenogenesis exhibit smaller testes and reduced fertility. [90]

    Mammals Edit

    There are no known cases of naturally occurring mammalian parthenogenesis in the wild. Though claims of that happening date back to antiquity, including in humans (for example, Virgin Mary, mother of Jesus), this has never been observed in a controlled environment. Parthenogenetic progeny of mammals would have two X chromosomes, and would therefore be female.

    In 1936, Gregory Goodwin Pincus reported successfully inducing parthenogenesis in a rabbit. [91]

    In April 2004, scientists at Tokyo University of Agriculture used parthenogenesis successfully to create a fatherless mouse. Using gene targeting, they were able to manipulate two imprinted loci H19/IGF2 and DLK1/MEG3 to produce bi-maternal mice at high frequency [92] and subsequently show that fatherless mice have enhanced longevity. [93]

    Induced parthenogenesis in mice and monkeys often results in abnormal development. This is because mammals have imprinted genetic regions, where either the maternal or the paternal chromosome is inactivated in the offspring in order for development to proceed normally. A mammal created by parthenogenesis would have double doses of maternally imprinted genes and lack paternally imprinted genes, leading to developmental abnormalities. It has been suggested [94] that defects in placental folding or interdigitation are one cause of swine parthenote abortive development. As a consequence, research on human parthenogenesis is focused on the production of embryonic stem cells for use in medical treatment, not as a reproductive strategy.

    Use of an electrical or chemical stimulus can produce the beginning of the process of parthenogenesis in the asexual development of viable offspring. [95]

    During oocyte development, high metaphase promoting factor (MPF) activity causes mammalian oocytes to arrest at the metaphase II stage until fertilization by a sperm. The fertilization event causes intracellular calcium oscillations, and targeted degradation of cyclin B, a regulatory subunit of MPF, thus permitting the MII-arrested oocyte to proceed through meiosis.

    To initiate parthenogenesis of swine oocytes, various methods exist to induce an artificial activation that mimics sperm entry, such as calcium ionophore treatment, microinjection of calcium ions, or electrical stimulation. Treatment with cycloheximide, a non-specific protein synthesis inhibitor, enhances parthenote development in swine presumably by continual inhibition of MPF/cyclin B. [96] As meiosis proceeds, extrusion of the second polar is blocked by exposure to cytochalasin B. This treatment results in a diploid (2 maternal genomes) parthenote [94] Parthenotes can be surgically transferred to a recipient oviduct for further development, but will succumb to developmental failure after ≈30 days of gestation. The swine parthenote placentae often appears hypo-vascular: see free image (Figure 1) in linked reference. [94]

    Humans Edit

    On June 26, 2007, International Stem Cell Corporation (ISCC), a California-based stem cell research company, announced that their lead scientist, Dr. Elena Revazova, and her research team were the first to intentionally create human stem cells from unfertilized human eggs using parthenogenesis. The process may offer a way for creating stem cells that are genetically matched to a particular female for the treatment of degenerative diseases that might affect her. In December 2007, Dr. Revazova and ISCC published an article [97] illustrating a breakthrough in the use of parthenogenesis to produce human stem cells that are homozygous in the HLA region of DNA. These stem cells are called HLA homozygous parthenogenetic human stem cells (hpSC-Hhom) and have unique characteristics that would allow derivatives of these cells to be implanted into millions of people without immune rejection. [98] With proper selection of oocyte donors according to HLA haplotype, it is possible to generate a bank of cell lines whose tissue derivatives, collectively, could be MHC-matched with a significant number of individuals within the human population.

    On August 2, 2007, after an independent investigation, it was revealed that discredited South Korean scientist Hwang Woo-Suk unknowingly produced the first human embryos resulting from parthenogenesis. Initially, Hwang claimed he and his team had extracted stem cells from cloned human embryos, a result later found to be fabricated. Further examination of the chromosomes of these cells show indicators of parthenogenesis in those extracted stem cells, similar to those found in the mice created by Tokyo scientists in 2004. Although Hwang deceived the world about being the first to create artificially cloned human embryos, he did contribute a major breakthrough to stem cell research by creating human embryos using parthenogenesis. [99] The truth was discovered in 2007, long after the embryos were created by him and his team in February 2004. This made Hwang the first, unknowingly, to successfully perform the process of parthenogenesis to create a human embryo and, ultimately, a human parthenogenetic stem cell line.

    Helen Spurway, a geneticist specializing in the reproductive biology of the guppy, Lebistes reticulatus, claimed, in 1955, that parthenogenesis, which occurs in the guppy in nature, may also occur (though very rarely) in the human species, leading to so-called "virgin births". This created some sensation among her colleagues and the lay public alike. [100] Sometimes an embryo may begin to divide without fertilisation but it cannot fully develop on its own, so while it may create some skin and nerve cells, it cannot create others (such as skeletal muscle) and becomes a type of benign tumor called an ovarian teratoma. [101] Spontaneous ovarian activation is not rare and has been known about since the 19th century. Some teratomas can even become primitive fetuses (fetiform teratoma) with imperfect heads, limbs and other structures but these are non-viable. However, in 1995 there was a reported case of partial-parthenogenesis a boy was found to have some of his cells (such as white blood cells) to be lacking in any genetic content from his father. Scientists believe that in the boy's case, an unfertilised egg began to self-divide but then had some (but not all) of its cells fertilised by a sperm cell this must have happened early in development, as self-activated eggs quickly lose their ability to be fertilised. The unfertilised cells eventually duplicated their DNA, boosting their chromosomes to 46. When the unfertilised cells hit a developmental block, the fertilised cells took over and developed that tissue. The boy had asymmetrical facial features and learning difficulties but was otherwise healthy. This would make him a parthenogenetic chimera (a child with two cell lineages in his body). [102] While over a dozen similar cases have been reported since then (usually discovered after the patient demonstrated clinical abnormalities), there have been no scientifically confirmed reports of a non-chimeric, clinically healthy human parthenote (i.e. produced from a single, parthenogenetic-activated oocyte). [101]

    Gynogenesis Edit

    A form of asexual reproduction related to parthenogenesis is gynogenesis. Here, offspring are produced by the same mechanism as in parthenogenesis, but with the requirement that the egg merely be stimulated by the presence of sperm in order to develop. However, the sperm cell does not contribute any genetic material to the offspring. Since gynogenetic species are all female, activation of their eggs requires mating with males of a closely related species for the needed stimulus. Some salamanders of the genus Ambystoma are gynogenetic and appear to have been so for over a million years. It is believed [ by whom? ] that the success of those salamanders may be due to rare fertilization of eggs by males, introducing new material to the gene pool, which may result from perhaps only one mating out of a million. In addition, the amazon molly is known to reproduce by gynogenesis. [103]

    Hybridogenesis Edit

    Hybridogenesis is a mode of reproduction of hybrids. Hybridogenetic hybrids (for example AB genome), usually females, during gametogenesis exclude one of parental genomes (A) and produce gametes with unrecombined [104] genome of second parental species (B), instead of containing mixed recombined parental genomes. First genome (A) is restored by fertilization of these gametes with gametes from the first species (AA, sexual host, [104] usually male). [104] [105] [106]

    So hybridogenesis is not completely asexual, but instead hemiclonal: half of genome is passed to the next generation clonally, unrecombined, intact (B), other half sexually, recombined (A). [104] [107]

    This process continues, so that each generation is half (or hemi-) clonal on the mother's side and has half new genetic material from the father's side.

    This form of reproduction is seen in some live-bearing fish of the genus Poeciliopsis [105] [108] as well as in some of the Pelophylax spp. ("green frogs" or "waterfrogs"):


    Homoplasy and Convergent Evolution

    In the last few posts in this series, we introduced the concept that individual characteristics (such as individual gene sequences) may not always match the phylogeny, or species tree for a group of related organisms. Incomplete lineage sorting is one way for this to occur, but another is for similarities to arise through independent events. Such features would have the superficial appearance of being inherited from a common ancestor, but in fact would be examples of homoplasies (singular = homoplasy): features shared between species that were not inherited from a common ancestor.

    Birds of a feather

    One classic example of a homoplasy is powered flight in birds and (some) mammals (i.e. bats). The species tree for birds, bats and non-flying mammals (for example, mice) places all mammals together as more closely related to each other than any is to birds. In order to explain the shared feature of powered flight for bats and birds, then, one needs to model it as a homoplasy – as independent events arising on two separate lineages:

    The alternate explanation – that powered flight is homologous between bats and birds (and thus present in their last common ancestor) – would require that all mammals except for bats have lost this ability (to say nothing of the reams of DNA sequence data that support the above species tree). Beyond this evidence, there is also good reason from comparative anatomy to think that powered flight arose independently in bats and birds. Birds use feathers attached along the length of their forelimbs to provide lift. In contrast, bats use a membrane to form their wings, and this membrane is attached between their digits as well as to their body:

    Both solutions work well, but when we break down the larger trait of “powered flight” into its component parts, we see that though the trait as a whole is convergent, the underlying components are not. This observation further supports the conclusion that powered flight in birds and mammals arose separately.

    Homoplasy vs. homology

    We can illustrate an example of how a simple DNA sequence homoplasy arises using a phylogeny. Suppose three species have the following sequence for a portion of the same gene:

    Based on these data alone, the simplest (most parsimonious) phylogeny would be as follows:

    Based on these data, the ancestral sequence would be inferred to be “TCATCC”, and the branch of the phylogeny leading to Species A would have one mutation to explain the observed sequence difference. In the absence of other evidence, this phylogeny would be the best fit for the data.

    This tidy picture, however, could be upset by more data – data that demonstrates that the simple species tree we have drawn above is in fact incorrect. If so, then we need to fit the above sequences into a different species tree – meaning that we will need to explain the pattern using more than one mutation event. Let’s work through a hypothetical example to show the process.

    Let’s suppose that sequence data for several hundred additional genes are compared for these three species, as well as for a number of other related species not shown in our species tree. Let’s also suppose that these data strongly support a different species tree than the one we just generated – in the vast, vast majority of cases, the data supports a tree with Species A and B as closest relatives, with Species C as more distantly related. This would “force” us to redraw the species tree as follows, placing our original short sequences into a different pattern along with their species:

    Let’s also suppose that the DNA sequence data for this particular gene sequence from the additional species not shown on the species tree indicate that the ancestral sequence actually had a “T” in the second position rather than a “C”:

    Now we have to account for all three species in our species tree having a non-ancestral sequence at the second position, as well as try to make sense of the mutation events that led to the pattern we see here. Note that we are still constrained to make the most parsimonious explanation for the whole of the data, but for this particular gene, we are forced to invoke multiple mutation events to fit the pattern to the species tree. We make this choice, however, because it would be even more unlikely for multiple mutation events to have shaped the pattern of the hundreds of other gene sequences in a coordinated fashion – and those other sequences support this version of the species tree.

    If you take the time to try “solving” the gene tree by adding mutation events to the species tree you’ll soon realize that at least three mutation events are needed to produce the observed pattern. There are also solutions that use more than three mutation events, but they are less likely explanations. One of the possible solutions is shown below:

    In the branch of the phylogeny leading to Species A and Species B, a (T to G) mutation occurs prior to the A / B divergence (represented by the red bar). A second mutation then occurs on the lineage leading to Species B that changes the G at the same position to a C (represented with a blue bar). Independently, the lineage leading to Species C also has a mutation at this position, changing the ancestral T to a C (also represented with a blue bar). The end result is that two of the sequences (in Species B and C) have become identical – but neither inherited the “C” at the second position from their common ancestor. In other words, they have arrived at the same “destination” from different starting points, or “converged” on a common sequence. Not surprisingly, this phenomenon is known as convergent evolution. For these two species, the “C” at the second position is not homologous (a similarity inherited from a common ancestor), but rather a homoplasy – a similarity that resulted from independent events on two lineages.

    Homoplasies can be as simple as single DNA monomer changes (as in this example), or as complex as the independent reorganization of multiple systems with numerous genes and body parts to converge on a solution (as in the case for powered flight in birds and bats). In both cases, however, we can determine that they arose as independent events on separate lineages because these features do not fit onto the species tree as unique events.

    The power of convergence

    Since homoplasies act as markers that flag repeated evolutionary events, looking for homoplasies in species trees is a useful way to test hypotheses about the reproducibility of evolution, or how often species converge on similar solutions. As it turns out, evolution is remarkably repeatable for many general traits. There are numerous examples of repeated, independent innovations over evolutionary history, some of which we will examine in more detail in upcoming posts:

    • Streamlined body shape: the streamlined body form of aquatic life such as fish, ichthyosaurs, whales, seals and diving birds (e.g. penguins) are all independent, convergent adaptations to an aquatic lifestyle.
    • Powered flight: in addition to birds and bats, powered flight also evolved independently in insects and pterodactyls.
    • Echolocation: some mammals, such as bats and whales, have independently developed systems that allow them to locate food through detecting how sound that they generate echoes off structures and prey in their environment.
    • Camera eyes: the repeated evolution of camera eyes (i.e. eyes that use a lens) is one of the most striking examples of convergent evolution. Camera eyes have independently evolved in cnidarians (certain jellyfish), cephalopods (such as squid and octopus) and vertebrates (birds, mammals).

    One thing to note is that these widespread examples of convergence are all shaped by the physical environment of the organisms in question – the perception of light (eyes), the ability to fly through air (wings), or move efficiently through water (streamlined body). The fixed presence of these environmental features would be expected to shape the adaptation of many species.

    Previously, we introduced the concept of a homoplasy – a similarity in form in two lineages that arises due to independent events. In the example we looked at last time, birds and bats independently obtained powered flight through convergent evolution – with bats arriving at membrane-based wings, and birds at feather-based wings. Since the last common ancestral population for bats and birds was a species that did not have powered flight, this is a good example of a homoplasy – one that arose through convergent evolution.

    Underneath this convergent event, however, there is a deeper connection. Bats and birds are both tetrapods – organisms with backbones and four limbs. The tetrapod body plan was already a feature of their last common ancestral population, and has been maintained in both lineages. As such, when considered strictly as a forelimb, bat wings and bird wings are homologous structures. In birds and bats, forelimbs have been shaped through natural selection for flight in different ways, but the starting point for both was a homologous structure. In other words, underneath the convergent event of powered flight in bats and birds is a deeper homology – the limb upon which both lineages independently constructed a wing. To represent this on a phylogeny, we would place the tetrapod body plan prior to the divergence of all tetrapods, and powered flight as two events on the appropriate lineages:

    This pattern – convergent events with deeper homologies lurking beneath them – is one that is seen time and again in evolution. In fact, these deeper homologies improve the odds that convergent events will occur, since they provide a common basis that separate lineages can use for independent innovation. For bats and birds, adaptations leading to flight were possible because both lineages had forelimbs that could be modified, over time, from one function to another. While this example is at the anatomical level, these sorts of “predispositions” and the convergent events that arise from them can be observed at the molecular level as well.

    The eyes have it

    As we mentioned in the previous post in this series, camera eyes are one of the most striking examples of convergent evolution, having appeared independently in several lineages (the most common examples of which are vertebrates, cephalopods such as octopus and squid, and certain jellyfish). Camera eyes have a light-sensitive cell layer (the retina) as well as a lens that focuses light on the retina. Explaining the distribution of camera eyes among these three groups requires us to invoke three convergent events on their phylogeny (“cnidarians” are the group in which jellyfish are found):

    At first glance, it seems wildly improbable that three distantly-related lineages would independently converge on such a remarkable structure as a camera eye. As it turns out, however, a key homology between all three groups greatly improved those odds – the molecules that act as light sensors.

    At its most basic form, sensing of the external environment requires that the environment induce a change within cells. Accordingly, sensing light requires a light-induced change of some kind. The key molecules that perform this function in all three of the above groups are proteins called opsins and their chemical partners (a group of compounds called retinals). Each opsin protein has a retinal attached to it, and together the opsin/retinal pair acts as a light sensor. Retinals change their shape when they interact with light (i.e. absorb a photon, represented by the gamma in the diagram below). This shape change in turn alters the shape of the opsin protein attached to the retinal:

    The change in shape of the opsin protein affects the flow of electrical charge in the cells responsible for sensing light, and these changes in electrical charge are what are perceived and interpreted by the brain as “light.”

    The opsin/retinal system of detecting light is a very widespread system – in fact, all animals that can detect light use these molecules as the physical basis for doing so, whether they have camera eyes or other eye types (such as compound eyes, or merely patches of light-sensitive cells). This is strong evidence that the opsin / retinal system predates the divergence of the three groups we are considering:

    With this knowledge in hand, we can see that the development of camera eyes in these lineages is not as improbable as we might have thought at first. In all three cases, these lineages built a camera eye around a preexisting molecular system for detecting light. The camera eyes themselves might be convergent, but they are based on a deeper underlying homology that improved the odds that they would appear through successive modifications of an ancestral system. And as we saw for bird and bat wings, there are differences between the camera eyes in these lineages that support the hypothesis that they are the result of convergent events (the most well-known example of which is that the vertebrate and cephalopod eyes have their nerve “wiring” in opposite orientations).

    Hearing is believing

    A second example of “molecular predisposition” leading to convergence can be seen in the molecular machinery underlying a different form of sensory perception – the ultrasonic hearing required for echolocation in bats and toothed whales. Both groups use highly tuned echolocation for navigation and seeking prey in an environment where visual perception is limited or lacking altogether. The evidence that the development of echolocation in these two very divergent groups of mammals is due to convergent evolution is strong – no other mammals more closely related to either group has such an ability.

    The cellular / molecular basis for detecting sound in mammals is a set of cells in the ear that extend hair-like projections (called cilia) that vibrate in response to different wavelengths of sound. Cilia also change their length and vibratory properties in response to different auditory stimuli. The vibrations are used to change the flow of electrical charge in these cells, eventually leading to nervous system signals that the brain perceives as sound. All mammals use a protein called prestin as part of the auditory system. Prestin is a “motor protein” that can change cell shape by moving internal structures around – and mammals use it for modifying cilia in response to sound.

    The cilia/prestin system is known to predate all mammals, so it is not surprising that toothed whales and bats use this system for hearing. What is interesting, however, is that in these groups the prestin protein has been independently shaped through natural selection to be tuned to high frequency (ultrasonic) sound more useful for echolocation. In fact, in a phylogeny restricted to prestin sequences, bat prestins and toothed whale prestins appear to be the most closely related to each other – a finding wildly at odds with the species tree for bats and whales. Further examination, however, shows that these striking similarities are the result of convergent evolution, not a more recent shared ancestry. In both cases, the prestin protein was available to become attuned to ultrasonic wavelengths, and similar (though not identical) mutation events in both lineages were selected for along the way – an additional example of a “deep homology” favoring independent convergent events.

    Summing up: evolution as a non-random process

    One common misconception I encounter about evolution is that it is predominantly a random process – one that is mainly influenced by chance events. While we have already shown that evolution has a strongly non-random component (natural selection), this discussion of convergent evolution further demonstrates that evolution is repeatable in certain important ways. When natural selection affects distantly-related groups in a similar fashion, we often observe similar outcomes. These similar outcomes are in many cases favored by prior history (homology) and arrived at through similar, but not identical paths (demonstrating that contingency and chance are present as well). Evolution is thus a balance of contingent events (mutations and other chance events) and emphatically non-contingent events (selection, convergent evolution).

    In the next post in this series, we’ll return to bat echolocation to explore how evolution of one species can be greatly shaped by another species in close relationship with it – a phenomenon known as coevolution.


    In mammals, what determines the average number of babies born during one pregnancy?

    Mammals like cats and dogs produce several babies while humans, on an average, produce only one baby during a pregnancy.

    Litter size seems to be determined by complex interactions of various factors. Indeed, even within the same species, litter size can vary considerably (as in the Arctic fox). Genetics plays somewhat of a role, as does a number of ecological factors like resource availability ("energy limitation hypothesis"), population density ("density variation hypothesis"), reproductive hormones acquired from eating prey ("hormone turbo hypothesis"), and environmental stability ("reproductive allocation hypothesis" and "jackpot hypothesis").

    There is also an element of maternal anatomy.

    In some species, the uterus is optimal for one baby at a time (humans, elephants). In other species the uterus is optimal for many (6 to 8 is frequent) babies at a time (pigs, cats, dogs, mice). Of course there is intraspecific variation (a woman could have triplets, and a cat could have only one kitten).

    There is generally a correlation between the optimal number of babies carried in the uterus and the number of teats.

    Generally, if gestation is long, the optimal number of babies will be lower than if gestation is short.


    Remingtonocetidae: Long-Snouted Cetaceans

    The oldest representatives of the Remingtonocetidae are found at the same fossil localities as Ambulocetus, but the greatest diversity of remingtonocetids is known from younger rocks, between 48 and 41 million years ago in India and Pakistan (Gingerich et al. 1997). In all, there are four or five genera of remingtonocetids, characterized by a long snout, which makes up nearly two thirds of the length of the skull.

    Dentally, remingtonocetids are specialized (Thewissen and Bajpai 2001a) their molars have lost the crushing basins of pakicetids and ambulocetids. This suggests that the diet of remingtonocetids is different from that of earlier cetaceans.

    In the genus Remingtonocetus, the eyes are very small (Thewissen and Nummela 2008), but the ears are large and set far apart on the skull, a feature that enhances directional hearing. In details of ear anatomy too, remingtonocetids are more specialized than pakicetids and ambulocetids (Nummela et al. 2007). One hearing-related feature is the size of the mandibular foramen, a perforation of the lower jaw behind the teeth. The foramen is enormous, covering nearly the entire depth of the jaw in modern cetaceans and remingtonocetids, unlike pakicetids, where it is smaller (Fig. 18). In all mammals, this foramen carries the nerves and blood vessels to the lower teeth and chin, but this does not account for its size in cetaceans. In modern cetaceans, this foramen carries, in addition to the nerves and blood vessels mentioned, a long pad of fat which connects the lower jaw to the middle ear and transmits underwater sounds. This pad was also present in remingtonocetids, suggesting that underwater sound transmission was effective in remingtonocetids, a clear aquatic adaptation (Nummela et al. 2007, 2004).

    Relative height of the mandibular foramen (mandibular foramen height divided by height of the mandible at the last tooth) in fossil cetaceans and modern odontocetes

    Remingtonocetids are also important because they document evolution in another major sense organ. The organ of balance is located in the petrosal, a bone attached to the ectotympanic. A major part of the organ of balance consists of three circular tubes, arranged in three planes that are at right angles to each other (Fig. 19). In general, the diameter of these tubes, the semicircular canals, scales with body size (Spoor and Thewissen 2008), but the canals are extremely reduced in modern cetaceans. The reason for this reduction is not fully understood, but it is possible that the reduction is related to the emergence of an immobile neck (Spoor et al. 2002). In mammals where it has been studied experimentally, a neural reflex, the vestibulocollic reflex, is engaged by stimulation of the semicircular canals and causes the neck muscles to contract and leads to the stabilization of the head, reducing the effect of sudden body movements on the head. Most modern cetaceans have a relatively stiff neck, and it is likely that this reflex, if present at all, cannot stabilize the head because the neck is already relatively immobile. This could then lead to overstimulation of the semicircular canals, especially in acrobatic animals. Reducing the size of the canals would reduce the chances of overstimulation and also limit the sensitivity of the canals. As such, it may give cetaceans the opportunity to be acrobatic. Remingtonocetids and all cetaceans higher on the cladogram have small canals, but pakicetids have large canals. The canals are not preserved in any Ambulocetus specimen.

    a Outline ellipses and regression of body size (on x-axis, as 10-log in grams) against semicircular canal radius (on y-axis, as 10-log in mm) for modern land mammals (maroon) and modern cetaceans (blue). Fossil cetaceans are the pakicetid Ichthyolestes (red), the remingtonocetid Remingtonocetus (orange), the protocetid Indocetus (yellow), and the basilosaurid Dorudon (purple). Modified from Spoor et al. (2002). b A reconstruction of inner ear of modern bowhead whale, showing semicircular canals above, broken stapes (yellow), and the cochlea below

    The morphology of the sense organs suggests that hearing was important for Remingtonocetus but that vision was not. This is consistent with the environmental evidence from the rocks that the fossils are found in. Indian Remingtonocetus probably lived in a muddy bay protected from the ocean by islands or peninsulas. Rivers may have brought sediment into this bay, and the water may not have been transparent.

    The postcranial skeleton of remingtonocetids (Bajpai and Thewissen 2000) shows that these whales had short legs but a very long powerful tail. Consistent with Fish's hypothesis regarding the evolution of cetacean locomotion, these cetaceans may have used their tail as the main propulsive organ in the water and only used their limbs for steering, and they were probably fast swimmers, although the semicircular canals indicate that there was limited ability for locomotion on land. Modern giant South American river otters (Pteronura brasiliensis) have a long tail that is flat dorsoventrally and that is swept up and down during swimming. This type of locomotion may be a good model for swimming in Remingtonocetus. Therefore, externally, remingtonocetids may have resembled enormous otters with long snouts (www.neoucom.edu/DEPTS/ANAT/Thewissen/whale_origins/whales/Remi.html).


    55 Q&As About the Human Circulatory System

    Poriferans, cnidarians, platyhelminthes and nematodes (nematodes have pseudocoelom fluid but no vessels) are avascular animals. Echinoderms do not have true circulatory systems either.

    3. What is the alternative means of substance transport in animals without a circulatory system? Why is blood important for larger animals?

    In animals that do not contain a circulatory system, the transport of substances occurs by cell to cell diffusion.

    Blood is a fundamental means of substance transport for larger animals since, in these animals, tissues are distant from each other and from the environment thus making diffusion impossible.

    Open and Closed Circulatory Systems

    4. What are the two types of circulatory systems?

    Circulatory systems can be classified into open circulatory systems and closed circulatory systems.

    5. What is an open circulatory system?

    An open circulatory system is one in which blood does not circulate only inside blood vessels but also flows into cavities that irrigate tissues. In open circulatory systems, blood pressure is low and generally the blood (called hemolymph) has a low level of cellularity.

    Arthropods, molluscs (cephalopods are exception) and protochordates have open circulatory systems.

    6. What is a closed circulatory system?

    A closed circulatory system is one in which blood circulates only inside blood vessels. For this reason, the blood pressure is higher in animals with closed circulatory systems. The cellularity of the blood is also higher, with many specific blood cells.

    Closed circulatory systems are a feature of annelids, cephalopod molluscs and vertebrates.

    7. What are the advantages of a closed circulatory system over an open circulatory system?

    A closed circulatory system is more efficient. Since blood circulates only inside blood vessels, it has a higher pressure and, as a result, can travel greater distances to the organs where hematosis happens and to peripheral tissues. In addition, the higher circulatory speed increases the animal’s capacity to distribute large supplies of oxygen to tissues that consume it in large amounts, such as muscle tissues, which can then perform faster movements. Animals with an open circulatory system (with the exception of insects, which carry out gas exchange separately from circulation) are generally slower and have a low metabolic rate.

    8. What is the difference between octopuses and mussels regarding their circulatory systems? How does that difference have an effect on the mobility of these animals?

    Cephalopod molluscs, such as octopuses and squids, have a closed circulatory system with blood pumped under pressure flowing within vessels. Bivalve molluscs, such as mussels and oysters, have an open circulatory system (also known as a lacunar circulatory system) where blood flows under low pressure, since it falls into cavities in the body and does not only circulate within blood vessels. Molluscs with closed circulatory systems are larger, agile and can actively move molluscs with open circulatory systems are smaller, slow and some are practically sessile.

    9. Why can flying insects such as flies beat their wings at a great speed despite having an open circulatory system?

    In insects, the circulatory system is open but this system does not participate in the gas exchange process or in oxygen supply to tissues. Gases enter and exit through the independent tracheal system, which allows for the direct contact of cells with theਊmbientਊir. Therefore, an insect can supply the large oxygen demand of its fast-beating wing muscles even though it has an open circulatory system.

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    The Components of the Circulatory System

    10. What are the typical components of a closed circulatory system?

    The typical components of a closed circulatory system are blood vessels within which blood circulates (arteries, veins and capillaries), a pumping organ (heart) and blood or਋loodlikeਏluid.

    11. How does the heart pump blood?

    The heart is a muscular organ that contains chambers (right atrium and right ventricle and left atrium and left ventricle) through which blood passes. The blood enters the heart in the atria, goes to the ventricles and then leaves the organ.

    The blood is pumped out of the heart by the contraction of the muscle fibers that form the ventricular walls. The contraction reduces the volume of ventricle, thus increasing the internal pressure and forcing the blood to flow to the exit vessels (the pulmonary artery for the right ventricle and the aorta for the left ventricle). When ventricular muscle fibers expand, the ventricles regain their original size and receive new blood flow from the atria.

    12. What is the difference between systole and diastole?

    Systole and diastole are the two stages into which the cardiac cycle is divided. Systole is the stage when the contraction of ventricular muscle fibers occurs and the ventricles are emptied. Diastole is the stage of the cardiac cycle when the ventricular muscle fibers expand and the ventricles are filled with blood.

    13. What are arterial vessels, arteries and arterioles?

    Arterial vessels are every blood vessel that carries blood from the heart to tissues. Arteries and arterioles are arterial vessels. Arterioles are thin arteries that end in capillaries.

    However, not all arteries contain arterial blood (highly oxygenated blood). The pulmonary artery and its branches, arteries that carry blood from the right heart ventricle to the lungs, contain venous blood.

    14. What are venous vessels, veins and venules?

    Venous vessels are every blood vessel that carries blood from tissues to the heart. Veins and venules are venous vessels. Venules are thin veins connected to capillaries.

    In general, venous vessels carry venous blood. However, the pulmonary veins that carry blood from the lungs to the left atrium of the heart contain arterial blood.

    15. What are the capillaries of the vascular system?

    Capillaries are small blood vessels that carry out the exchange of substances between the blood and body tissues. Capillaries are neither arteries nor veins since they have distinct features. In capillaries, the wall is made of a single layer of endothelial cells through which substances are exchanged. These vessels receive blood from arterioles and drain into venules.

    16. What part of the vascular system carries out the exchange of gases and other substances between tissues?

    Only capillaries carry out the exchange of gases and other substances between tissues.

    17. Which contain more muscle tissue, arteries or veins? How different are the walls of these two types of blood vessels?

    The arterial system has thicker muscle walls, since within arteries blood circulates under higher pressure. Veins are more flaccid than arteries.

    From the lumen to the external layer, both types of vessels are made of endothelium, muscle tissue and connective tissue. The endothelium of both is made up of a single layer of cells. In arteries, the muscle tissue portion is thicker than in veins whereas, in veins, the external connective tissue is thicker than in arteries.

    Arteries are pulsating blood vessels. The arterial pulse can be felt during a medical examination, for example, through the palpation of the radial artery in the internal-lateral face of the wrist near the base of the thumb.

    18. What are the valves of the venous system? What is their function?

    The valves of the venous system are structures inside veins that make it so that blood only flows in the right direction (from tissues to the heart). preventing it from going backwards in favor of gravity. The valves close when the pressure of the fluid column above (afterwards, in terms of normal flow) is higher than the fluid pressure below them. Valves are therefore necessary for the process of blood returning to the heart.

    19. How do the muscles of the legs and feet contribute to venous return?

    The muscles of the legs, and mainly the muscles of the calves, contract and compress the deep veins of the legs, pushing blood towards the heart.

    The plantar portion of the foot holds blood and, when it is pushed against the ground,  it pushes its blood volume back towards the heart and therefore aids in venous return.

    20. What are varices? Why are they more common on the lower limbs?

    A varix means is an abnormal enlargement of a vein. Varices occur when excessive pressure against the normal blood flow enlarges the vein and, as a result, causes its valves to stop working properly (venous insufficiency).

    Varices are more common in the veins of the lower limbs since the fluid column above these vessels is higher. This is the reason why people who spend a large amount of time standing (e.g., surgeons) are more likely to develop varices.

    In general, varices are not the superficial veins that can be seen on the legs of varix patients. These superficial veins are the result of internal varices (venous insufficiency) in the deep internal veins of the legs. These outer veins appear this way because blood flow is diverted from the internal veins to superficial ones. (However, superficial veins with this appearance are often called varices.)

    The Lymphatic System

    21. What is the lymphatic system?

    The lymphatic system is a network of specialized vessels with valves, which drains interstitial fluid (lymph). The lymphatic system is also responsible for the transport of chylomicrons (vesicles that contain lipids) produced after the absorption of fats by the intestinal epithelium.

    Along lymphatic vessels are ganglial-like structures called lymph nodes. which contain many immune system cells. These cells filter impurities and destroy microorganisms and cellular waste. The lymphatic vessels drain to two major lymphatic vessels, the thoracic duct and the right lymphatic duct, which in turn drain into tributary veins of the superior vena cava.

    22. Why may clinical signs regarding the lymphatic system be observed during inflammatory and infectious conditions?

    The lymph nodes, or lymph glands, have lymphoid tissue that produces lymphocytes (a type of leukocyte). In inflammatory and infectious conditions, it is common to see the enlargement of lymph nodes in the lymphatic circuits that drain the affected region due to the reactive proliferation of leukocytes. This enlargement is known as lymphadenomegaly and is sometimes accompanied by pain. Checking for enlarged or painful lymph nodes is part of medical examinations since these findings may suggest inflammation, infection or other diseases.

    Heart Structure, Heart Circulation and the Cardiac Cycle

    23. What chambers of the heart does blood enter? From which does it exit the heart? 

    The chambers of the heart through which blood enters are the atria. There heart contains a right atrium and a left atrium.

    The chambers of the heart through which blood exits are the ventricles. The heart contains a right ventricle and the a ventricle.

    24. Concerning the thickness of their walls, how different are the chambers of the heart?

    The walls of the ventricle are thicker than those of the atrium, since the ventricles are the structures responsible for the pumping of the blood to the lungs or tissues. The muscular work of the ventricles is harder and their muscle fibers are more developed.

    The left ventricle is more muscular than the right ventricle, because pumping blood to the lungs (the task of the right ventricle) is easier (an requires less pressure) than pumping blood to the other tissues of the body (the task of the left ventricle).

    25. What are the vena cava? What type of blood circulates within the vena cava?

    The vena cava are two large veins that empty into the right atrium. The superior vena cava drains all the blood that comes from the head, the upper limbs, the neck and the upper portion of the trunk. The inferior vena cava carries blood drained from the lower portion of the trunk and the lower limbs.

    Venous blood circulates within the vena cava.

    26. Which chamber of the heart does blood enter first? Where does blood go after passing through that chamber? What is the name of the valve that separates the chambers? Why is that valve necessary?

    Venous blood from tissues arrives at the right atrium of the heart. From the right atrium, the blood goes to the right ventricle. The valve that separates the right ventricle from the right atrium is the tricuspid valve (a valve system made of three leaflets). The tricuspid valve is necessary to prevent blood from returning to the right atrium during systole (the contraction of the ventricles).

    28. What is the name of the valve that separates the right ventricle from the pulmonary artery? Why is that valve important?

    The valve that separates the right ventricle from the base of the pulmonary artery is the pulmonary valve. The pulmonary valve is important in preventing blood from pulmonary circulation from flowing back into the heart during diastole.

    29. Do the arteries that carry blood from the heart to the lungs contain arterial or venous blood? What happens to blood when it passes through the lungs?

    Arteries of the pulmonary circulation carry venous blood and not arterial blood.

    When blood goes through the alveolar capillaries of the lungs, hematosis (oxygenation) occurs and carbon dioxide is released to the exterior.

    30. What are pulmonary veins? How many are there?

    Pulmonary veins are part of the pulmonary circulation. They are vessels that carry oxygen-rich (arterial) blood from the lungs to the heart. There are four pulmonary veins, two that drain blood from the right lung and two that drain the left lung. The pulmonary veins empty into the left atrium, supplying the heart with arterial blood. Although they are veins, they carry arterial blood and not venous blood.

    31. What chamber of the heart does blood enter after leaving the left atrium? What valve separates these chambers?

    The arterial blood that has gone from the lungs to the left atrium then goes on to the left ventricle.

    The valve between the left ventricle and the left atrium is the mitral valve, a bicuspid (two leaflets) valve. The mitral valve is important because it prevents blood from flowing back into the left atrium during systole (the contraction of the ventricles).

    32. What is the function of the left ventricle? Where does the blood go after leaving the left ventricle?

    The function of the left ventricle is to receive blood from the left atrium and to pump the blood under high pressure into circulation. After leaving the left ventricle, the blood enters the aorta, the largest artery of the body.

    Circulatory System Review - Image Diversity: the aorta

    33. What valve separates the aorta from the heart? What is the importance of that valve?

    The valve between the left ventricle and the aorta is the aortic valve. The aortic valve prevents blood from flowing back into the left ventricle during diastole. In addition, as the aortic valve closes during diastole, part of the reverse blood flux is pushed through the coronary ostia (openings), holes located in the aorta wall just after the valvular insertion and which are connected to the coronary circulation, which is responsible for supplying blood to cardiac tissues.

    34. Is ventricular lumen larger during systole or diastole?

    Systole is the stage of the cardiac cycle during which the ventricles contract. Therefore, the lumen of these chambers is reduced and the pressure on the blood within them is increased.

    During diastole, the opposite occurs. The muscle fibers of the ventricles relax and the lumen of these chambers enlarges, allowing the entrance of blood.

    35. During what stage of the cardiac cycle are the ventricles filled with blood?

    The ventricles are filled with blood during diastole. 

    How the human heart functions.Video by http://visiblebody.com/

    Posted by I fucking love science on Segunda, 12 de outubro de 2015

    36. What type of tissue is the heart composed of? How is this tissue oxygenated and supplied with nutrients?

    The heart is made of striated cardiac muscle tissue. The heart muscle is called the myocardium and it is oxygenated and supplied with nutrients by the coronary arteries. The coronary arteries come from the base of the aorta and branch out around the heart, penetrating the myocardium.

    Diseases of the coronary arteries are severe conditions.

    Gas Circulation, Hemoglobin and Erythropoietin

    37. What are the two main metabolic gases transported by blood?

    The main metabolic gases transported by blood are molecular oxygen (O₂) and carbon dioxide (CO₂).

    38. How do respiratory pigments work?

    Respiratory pigments are oxygen-carrying molecules present in blood. When the oxygen concentration is high, for example, in the pulmonary alveoli, respiratory pigments bind to the gas. In conditions of low oxygen concentration, such as in tissues, the respiratory pigments release the molecule.

    The respiratory pigment of human blood is hemoglobin, which is present within red blood cells.

    39. How different are oxyhemoglobin and hemoglobin? Where are you more likely to find a higher concentration of oxyhemoglobin, in peripheral tissues or in the lungs?

    Oxygen-bound hemoglobin is called oxyhemoglobin. In the lungs, the oxygen concentration is higher and, as a result, there is a higher concentration of oxyhemoglobin . In peripheral tissues, the situation is the reverse, as the concentration of oxygen is lower and there is more free hemoglobin.

    40. What is hemoglobin F? Why does the fetus need a different type of hemoglobin?

    Hemoglobin F is the hemoglobin found in the fetus of mammals whereas hemoglobin A is normal hemoglobin. Hemoglobin F has a greater affinity to bind to oxygen.

    The fetus needs hemoglobin capable of extracting oxygen from the mother’s blood. Therefore, the fetus uses hemoglobin F since it has greater affinity for oxygen than the mother’s hemoglobin.

    41. At high altitudes, is it necessary for blood to contain more or less hemoglobin?

    At high altitudes, the air has lower pressure and the concentration of oxygen is lower than at low altitudes. In this situation, the efficiency of the respiratory system must be greater and therefore the body synthesizes more hemoglobin (and more red blood cells) in an attempt to obtain more oxygen. This phenomenon is known as compensatory hyperglobulinemia.

    Compensatory hyperglobulinemia is the reason why athletes who will compete at high altitudes need to arrive there a few days before the event so that there is time for their body to make more red blood cells, thus allowing them to be less affected by the effects of the low atmospheric oxygen concentration (fatigue, reduced muscular strength).

    42. What substance stimulates the production of red blood cells? Which organ secretes it? Under what conditions is it secreted at higher rates?

    The substance that stimulates the production of red blood cells by the bone marrow is erythropoietin. Erythropoietin is a hormone secreted by the kidneys. Its secretion is increased when there is a deficiency in tissue oxygenation (tissue hypoxia) caused by either reduced oxygen availability (as is the case at high altitudes) or by internal diseases, such as pulmonary diseases.

    43. Why is carbon monoxide toxic to humans?

    Hemoglobin “likes” carbon monoxide (CO) much more than it likes oxygen. When carbon monoxide is present in the inhaled air, it binds to hemoglobin to form carboxyhemoglobin by occupying the binding site where oxygen would normally bind. Due hemoglobin's greater affinity for carbon monoxide (for example, in intoxication from car exhaust) there is no transportation of oxygen and the individual undergoes hypoxia, loses consciousness, inhales more carbon monoxide and may even die.

    Intoxication by carbon monoxide is an important cause of death in fires and closed garages.

    44. During what stage of cellular respiration is carbon dioxide released?

    In aerobic cellular respiration, the release of carbon dioxide happens during the transformation of pyruvic acid into acetyl-CoA (two molecules) and during the Krebs cycle (four molecules). For each glucose molecule, six carbon dioxide molecules are produced.

    45. How is carbon dioxide released by cellular respiration transported from tissues to be eliminated through the lungs?

    In vertebrates, almost 70% of this carbon dioxide is transported by the blood in the form of bicarbonate, 25% is bound to hemoglobin, and 5% dissolved in the plasma.

    Circulation in Other Animals

    46. What is the difference between double closed circulation and simple closed circulation?

    Double closed circulation, or closed circulation, is that when blood circulates through two associated and parallel vascular systems: one that carries blood to peripheral tissues and transports aways from them (systemic circulation) and another that carries blood to the tissues that perform gas exchange with the environment (pulmonary circulation) and then transport this blood way from them. Double circulation occurs in amphibians, reptiles, birds and mammals.

    Simple closed circulation, or simple circulation, is when the tissues that perform gas exchange are connected in series to the systemic circulation, such as in fish.

    47. How many chambers does the fish heart have?

    The fish heart is a tube made of two consecutive chambers: one atrium and one ventricle.

    48. Does the fish heart pump venous or arterial blood?

    The venous blood from tissues enters the atrium and goes on to the ventricle, which then pumps the blood towards the gills. After oxygenation in the gills, the arterial blood goes to the tissues. Therefore, the fish heart pumps venous blood.

    49. Why is the circulatory system of fish classified as simple and complete circulation?

    Complete circulation is when there is no mixture of venous and arterial blood. Simple circulation is when blood circulates only in one circuit (as opposed to double circulation, which contains two circuits, the systemic circulation and pulmonary circulation). In fish, the circulatory system is simple and complete.

    50. How many chambers does the amphibian heart have?

    The amphibian heart has three heart chambers: two atria and one ventricle.

    51. Why can amphibian circulation be classified as double and incomplete?

    Amphibian circulation is double because it consists of systemic and pulmonary circulation: that is, heart-tissues-heart and heart-lungs-heart, respectively. Since amphibians have only one ventricle in their heart, venous blood taken from the tissues and arterial blood coming from the lungs are mixed in the ventricle, which then pumps the mixture back into systemic and pulmonary circulations. Amphibian circulation is considered incomplete because venous and arterial blood mix in the circuit.

    Blood oxygenation in amphibians also occurs in systemic circulation, since their skin is a gas exchange organ.

    52. What is the difference between the amphibian heart and the reptile heart?

    Reptiles also have double and incomplete circulation, with a heart that contains three chambers (two atria and one ventricle). However, the reptile heart presents the beginning of a ventricular septation that partially separates the right and left region of the chamber. With this partial ventricular septation, there is less mixture of arterial with venous blood among reptiles than among amphibians.

    53. How many chambers do the hearts of birds and mammals have? Concerning temperature maintenance, what is the advantage of the double and complete circulation of these animals?

    Bird and mammal hearts are divided into four chambers: the right atrium, the right ventricle, the left atrium and the left ventricle.

    Birds and mammals are homeothermic, meaning that they control their body temperature. Their four-chambered heart and double circulation provide tissues with more oxygenated blood, making a higher metabolic rate possible (mainly cellular respiration rate). Part of the energy produced by cellular respiration is used to maintain body temperature.

    54. Concerning the mixture of arterial with venous blood, what is the difference between human fetal circulation and adult circulation?

    In human fetal circulation, there are two points at which arterial and venous blood are mixed, which characterizes this as an incomplete circulation. One of them is the oval foramen, an opening between the right and the left atria of the fetal heart. The other is the arterial duct, a short vessel that connects the pulmonary artery to the aorta. These points close a few days after birth and as a result are not present in the adult heart.

    Heart Conduction

    55. What causes the heart to contract?

    Heart contraction is independent from neural stimulus (although it can be regulated by the autonomous nervous system). The heart contains pacemaker cells that independently trigger the action potentials that begin muscle contraction. These cells are concentrated at two special points in the heart: the sinoatrial node (SA node), located in the upper portion of the right atrium, and the atrioventricular node (AV node), located near the interatrial septum.

    The action potentials generated by the depolarization of SA node cells propagate from cell to cell throughout the atria, producing the atrial contraction. The atrial depolarization also propagates to the AV node, which then transmits the electric impulse to the ventricles through specialized conduction bundles of the interventricular septum (the bundle of His) and then to the Purkinje fibers of the ventricle walls, causing a ventricular contraction. (Atrial contraction precedes ventricular contraction so that blood fills the ventricles before ventricular contraction.)

    The repolarization of the SA node makes the atria relax, with the ventricles relaxing afterwards.

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    How Diving Mammals Stay Underwater for So Long

    Positive charges on oxygen-binding proteins are key to diving mammals' success.

    Imagine holding your breath while chasing down a giant squid (Architeuthis dux)—multi-tentacled monsters wielding suckers lined with tiny teeth—in freezing cold water, all in the dark. That would take a lot out of anybody, yet sperm whales (Physeter macrocephalus) do this day in and day out.

    The ability to dive underwater for extended periods is a specialized feat marine and aquatic mammals have evolved over millions of years. Diving mammals will slow their heart rate, stop their breathing, and shunt blood flow from their extremities to the brain, heart, and muscles when starting a dive. (Related: "Can Diving Mammals Avoid the Bends?")

    But champion divers, such as elephant seals, can hold their breath for about two hours. "It was known that they rely on internal oxygen stores when they're down there," said Michael Berenbrink, a zoologist at the University of Liverpool, England, who specializes in how animals function.

    But there was something else going on in the bodies of these animals that researchers were missing, until now.

    So what's new? A study published June 13 in the journal Science reports that diving mammals—including whales, seals, otters, and even beavers and muskrats—have positively charged oxygen-binding proteins, called myoglobin, in their muscles.

    This positive characteristic allows the animals to pack much more myoglobin into their bodies than other mammals, such as humans—and enables diving mammals to keep a larger store of oxygen on which to draw while underwater.

    Why is it important? Packing too many proteins together can be problematic, explained Berenbrink, a study co-author, because they clump when they get too close to each other.

    "This [can cause] serious diseases," he added. In humans, ailments like diabetes and Alzheimer's can result.

    But myoglobin is ten times more concentrated in the muscles of diving mammals than it is in human muscles, Berenbrink said.

    Since like charges repel each other—think of trying to push together the sides of two magnets with the same charge—having positively charged myoglobin keeps the proteins from sticking to each other.

    What does this mean? Berenbrink and colleagues found this positive charge in the myoglobin of all the diving mammals they examined, although some had larger positive charges than others.

    This study provides a nice example of convergent evolution—where different lineages living in similar environments evolve the same answer to a common problem, wrote Randall Davis, a biologist who studies the physiology and behavior of marine birds and mammals at Texas A&M University in Galveston, in an email.

    "[And it] sheds light on the origins of myoglobin and its role in extending breath-hold duration in aquatic mammals," said Davis, who was not involved in the study.

    "It will raise some controversy, but at the same time I think it's going to stimulate more research, which I couldn't be more pleased about," said Jerry Kooyman, an animal physiologist at the Scripps Institution of Oceanography in San Diego who was not involved in the study.

    Kooyman cautions that some of what’s known about aspects of diving behavior, such as dive duration, is based on small sample sizes. So researchers must be careful when trying to draw connections between diving ability and how much myoglobin a species can claim.

    What's next? Berenbrink hopes to look at the myoglobin in humans from societies with a history of diving behavior to see if they show similar changes in their oxygen-binding protein.

    "There are ethnic groups around the world who have relied on diving to get food. Some of these humans can stay underwater for a very long time," he said.