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Sexual Distortion

  • Writer: Lafyva
    Lafyva
  • May 20, 2019
  • 27 min read

Updated: Aug 10

Marcus Aurelius "sex is the friction of a piece of gut and, following a sort of convulsion, the expulsion of some mucus"









There are other forms of asexual reproduction in animals that are

more complex. For example, a hermaphrodite is an animal that has

both male and female reproductive organs in the same individual.

Thus, these creatures can potentially mate with every individual they

meet from the same species. Most hermaphrodites in the animal

kingdom are invertebrates. There are only a few hermaphrodites

among thousands of species of insects. But there are many

hermaphroditic worms.



Decided on June 26, 2015, Obergefell overturned Baker and requires all states to issue marriage licenses to same-sex couples and to recognize same-sex marriages validly performed in other jurisdictions.[4] This established same-sex marriage throughout the United States and its territories.


In addition, about 60 per cent of the pre-adolescent boys engage in homosexual activities


a broader debate emerged on the issue of gay civil rights, and an increase in scientific studies on biology of sexual orientation. As Lewis(2009) indicated, we cannot establish definitive causation


This article critically reviews that "scientific evidence" and finds that much of their literature does not support the claim that homosexuality is normal. This article suggests that instead of supporting their claim with scientific evidence, those major medical associations arbitrarily label homosexuality as normal.

Untreated MtFs and FtMs who have an early onset of their gender dysphoria and are sexually oriented to persons of their natal sex show a distinctive brain morphology, reflecting a brain phenotype. These phenotypes are different from those of heterosexual males or females

The gender identity/gender dysphoria questionnaire for adolescents and adults

Validation of the Chinese Version of the Gender Identity/Gender Dysphoria Questionnaire for Adolescents and Adults




[(Death/severe defect for full siblings 40.3%)(Normal: 44.5%)] Cousin 1/4 risk



Author Summary

Southern Europeans and Middle Eastern populations are known to have inherited a small percentage of their genetic material from recent sub-Saharan African migrations, but there has been no estimate of the exact proportion of this gene flow, or of its date. Here, we apply genomic methods to show that the proportion of African ancestry in many Southern European groups is 1%–3%, in Middle Eastern groups is 4%–15%, and in Jewish groups is 3%–5%. To estimate the dates when the mixture occurred, we develop a novel method that estimates the size of chromosomal segments of distinct ancestry in individuals of mixed ancestry. We verify using computer simulations that the method produces useful estimates of population mixture dates up to 300 generations in the past. By applying the method to West Eurasians, we show that the dates in Southern Europeans are consistent with events during the Roman Empire and subsequent Arab migrations. The dates in the Jewish groups are older, consistent with events in classical or biblical times that may have occurred in the shared history of Jewish populations.


Mummy DNA unravels ancient Egyptians’ ancestry


No evidence of Neandertal admixture in the mitochondrial genomes of early European modern humans and contemporary Europeans

The fact that the Neandertal Y-chromosome lineage we describe has never been observed in modern humans suggests that the lineage is most likely extinct. Although the Neandertal Y chromosome (and mtDNA) might have simply drifted out of the modern human gene pool,24 it is also possible that genetic incompatibilities contributed to their loss.


Ancient DNA and the rewriting of human history: be sparing with Occam’s razor




The Genomic Signature of Inequality
In humans, the profound biological differences that exist between the sexes mean that a single male is physically capable of having far more children than is a single female. Women carry unborn children for nine months and often nurse them for several years prior to having additional children.13 Men, meanwhile, are able to procreate while investing far less time in the bearing and early rearing of each child, a biological difference whose effects are amplified by social factors such as the fact that in many societies, men are expected to spend little time with their children. So it is that, as measured by the contribution to the next generation, powerful men have the potential to have a far greater impact than powerful women, and we can see this in genetic data.
When I started my first academic job in 2003, I bet my career on the idea that the history of mixture of West Africans and Europeans in the Americas would make it possible to find risk factors that contribute to health disparities for diseases like prostate cancer, which occurs at about a rate 1.7 times higher in African Americans than in European Americans.1 This particular disparity had not been possible to explain based on dietary and environmental differences across populations, suggesting that genetic factors might play a role. African Americans today derive about 80 percent of their ancestry from enslaved Africans brought to North America between the sixteenth and nineteenth centuries. In a large group of African Americans, the proportion of African ancestry at any one location in the genome is expected to be close to the average (defining the proportion of African ancestry as the fraction of ancestors that were in West Africa before around five hundred years ago). However, if there are risk factors for prostate cancer that occur at higher frequency in West Africans than in Europeans, then African Americans with prostate cancer are expected to have inherited more African ancestry than the average in the vicinity of these genetic variations. This idea can be used to pinpoint disease genes. To make such studies possible, I set up a molecular biology laboratory to identify mutations that differed in frequency between West Africans and Europeans. My colleagues and I developed methods that used information from these mutations to identify where in the genome people harbor segments of DNA derived from their West African and European ancestors. To prove that these ideas worked in practice, we applied them to many traits, including prostate cancer, uterine fibroids, late-stage kidney disease, multiple sclerosis, low white blood cell count, and type 2 diabetes. In 2006, my colleagues and I applied our methods to 1,597 African American men with prostate cancer, and found that in one region of the genome, they had about 2.8 percent more African ancestry than the average in the rest of their genomes. The odds of seeing a rise in African ancestry this large by accident were about ten million to one. When we looked in more detail, we found that this region contained at least seven independent risk factors for prostate cancer, all more common in West Africans than in Europeans. Our findings could account entirely for the higher rate of prostate cancer in African Americans than in European Americans. We could conclude this because African Americans who happen to have entirely European ancestry in this small section of their genomes had about the same risk for prostate cancer as random European Americans.
In 2008, I gave a talk about my work on prostate cancer to a conference on health disparities across ethnic groups in the United States. In my talk, I tried to communicate my excitement about the scientific approach and my conviction that it could help to find genetic risk factors for other diseases. Afterward, though, I was angrily questioned by an anthropologist in the audience, who believed that by studying “West African” or “European” segments of DNA to understand biological differences between groups, I was flirting with racism. Her questions were seconded by several others, and I encountered similar responses at other meetings. A legal ethicist who heard me talk on a similar theme suggested that I might want to refer to the populations from which African Americans descend as “cluster A” and “cluster B.” But I replied that it would be dishonest to disguise the model of history that was driving this work. Every feature of the data I looked at suggested that this model was a scientifically meaningful one, providing accurate estimates of where in the genome people harbor segments of DNA from ancestors who lived in West Africa or in Europe in the last twenty generations, prior to the mixture caused by colonialism and the slave trade. It was also clear that the approach was identifying real risk factors for disease that differ in frequency across populations, leading to discoveries with the potential to improve health.
Neanderthal mitochondrial DNA provided no support for the theory that Neanderthals and modern humans interbred when they encountered each other, but at the same time the mitochondrial DNA evidence could not exclude up to around a 25 percent contribution of Neanderthals to the DNA of present-day non-Africans. There is a reason why we have so little power to make statements about the Neanderthal contribution to modern humans based only on mitochondrial DNA. Even if modern humans outside Africa today do have substantial Neanderthal ancestry, there are only one or few women who lived at that time and were lucky enough to pass down their mitochondrial DNA to present-day people, and if most of those women were modern humans, the patterns we see today would not be surprising. So the mitochondrial data were not conclusive, but nevertheless the view that Neanderthals and modern humans did not mix remained the scientific orthodoxy until Svante Pääbo’s team extracted DNA from the whole genome of a Neanderthal, making it possible to examine the history of all its ancestors, not just the exclusively maternal line.
Denisovans were genetically a little closer to New Guineans than they were to any population from mainland Eurasia, suggesting that New Guinean ancestors had interbred with Denisovans. Yet the distance from Denisova Cave to New Guinea is around nine thousand kilometers, and New Guinea is, of course, separated by sea from the Asian mainland. The climate in New Guinea is also largely tropical, which could not be more different from Siberia’s bitter winters, and this makes it unlikely that archaic humans adapted to one environment would have flourished in the other.




A wealth of data confirms that genetic variation is an important determinant of multiple sclerosis (MS) risk. Population, family and molecular studies provide strong empirical support for a polygenic model of inheritance, driven primarily by allelic variants relatively common in the general population. The major histocompatibility complex (MHC) in chromosome 6p21.3 represents by far the strongest MS susceptibility locus genome-wide and was unambiguously identified in all studied populations.

The first MS-associated genetic risk locus discovered in 1972 was located in the human leukocyte antigen (HLA) class I region on chromosome 6

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, with a strong genetic component.

The MHC loci on chromosome 6 is a crucial predisposing factor for number of auto immune diseases (Vasiliki, Vinod, et al., 2017).






MHC MOLECULES Major Histocompatibility Complex (MHC) is a large group of genes, including those encoding the class I and II MHC molecules, involved in the presentation of antigen to T cells. The complex was originally identified as a locus encoding allogeneic cell-surface molecules involved in graft rejection. A variety of other proteins are also encoded in the MHC, including complement components (C4, C2,FB), heat shock proteins, and cytokines (TNFα, TNFβ). MHC class I molecules are integral membrane proteins found on all nucleated cells and platelets. They are the classical transplantation antigens, each having one polypeptide chain encoded within the MHC that traverses the plasma membrane. The extracellular portion has three domains (α1–α3). The membrane-proximal α3 domain is associated with β2-microglobulin, whereas the two N-terminal domains form an antigen-binding pocket, consisting of a base of β-pleated sheet derived from both α1 and α2 domains, surrounded by two loops of α helix. Residues facing into the binding pocket vary between different molecules and haplotypes, to allow different antigenic peptides to bind. The α3 domain has a binding site for CD8. β2-microglobulin (β2m) is a polypeptide encoded by a gene outside the MHC, which forms a single domain related to Ig domains. It is necessary for loading and transport of class I to the cell surface. Class I-like (nonclassical) MHC molecules have the same basic structure as MHC class I molecules, and a variety of functions. Some are encoded within the MHC, but many are not. CD1 is a group of four MHC class I-like molecules with deep antigen-binding pockets that can accommodate acyl groups of lipoprotein and glycolipid antigens, such as lipoarabinomannan from mycobacteria, which they present to T cells. MHC class II molecules are expressed on B cells, macrophages, monocytes, dendritic cells, APCs, and some T cells. They consist of two noncovalently linked polypeptides (α and β), both encoded within the MHC, which both traverse the plasma membrane, each having two extracellular domains. Class II molecules resemble class I molecules with the N-terminal α1 and β1 domains forming the peptide-binding site. Another site in the β2 domain binds to CD4. Several class II-like genes (DM) are also encoded in the MHC. They facilitate the loading of antigenic peptides onto the class II molecules. MHC GENES A major histocompatibility complex (MHC) is found in all mammal species. In humans the locus is called HLA; in mice it is the H-2 complex and in rats it is RT-1. HLA (Human Leukocyte Antigen) locus is the human MHC, socalled because the MHC molecules were originally identified as antigens on the surface of leukocytes and genetic variability in the MHC molecules was identified serologically. Nowadays variations are identified by genotyping. The HLA complex contains more than 220 individual gene loci, of which 21 have an immunological function. The class I and class II genes are highly polymorphic, with more than 6000 class I sequence variants and 1500 class II variants identified. There is also some variation in copy number in individual loci between haplotypes. The gene complex is located on chromosome 6, and it includes three principal class I and three class II loci. HLA-A, -B, and -C loci encode the α chains of the classical MHC class I molecules, expressed by all nucleated cells, which present antigens to CD8+ cytotoxic T cells. HLA-E encodes a class I-like molecule that presents the signal sequence (leader) peptides of the classical MHC class I molecules to NK cells. The complex is recognized by a receptor consisting of CD94 and NKG2. HLA-E genes have limited polymorphism. HLA-G is a class I-like molecule expressed on the placental syncytiotrophoblasts (which do not express HLA-A, -B, and -C) and is thought to prevent allograft rejection of the fetus mediated by NK cells. It can be produced in membrane-bound and soluble forms. b HLA-DP, -DQ, and -DR loci encode class II MHC molecules expressed on APCs, which present peptides to CD4+ T cells. Originally these were described as HLA-D specificities, detected by their ability to stimulate allogeneic cells in mixed lymphocyte cultures. Later they were defined serologically and most recently by gene sequence. DP and DQ each encode one pair of class II α and β chains, plus pseudogenes. The DR locus encodes one α chain and one to four β chains depending on the individual haplotype. Since α chains encoded on one chromosome can combine with β chains encoded on the other, this is a source of additional structural diversity in class II molecules. HLA-DM encodes the class II molecule DM, which is involved in loading peptides onto class II molecules. LMP-2 and LMP-7 encode components of proteasomes which are induced by interferon-γ and modify the proteasome function. TAP-1 and TAP-2 encode transporters that take antigenic peptides from the cytoplasm into the endoplasmic reticulum (ER). HLA-class III genes is a catch-all term for other genes encoded within the MHC, including complement components C2 and FB, the pseudoalleles for C4 (C4F and C4S), which determine the Rogers and Chido blood groups, respectively. Genes for TNF, some heat shock proteins (e.g., HSP7), two of the natural cytotoxicity receptors and enzymes (e.g., adrenal steroid 21-hydroxylase, CYP21) lie in this region. H-2 is the mouse MHC, which lies on chromosome 17. There are six main regions: K, M, A, E, S, and D. H-2K and H-2D encode class I MHC molecules. The K locus has one gene, whereas the number of genes in the D locus varies between strains. H-2A and H-2E encode the α and β chains of the class II molecules. This was previously designated as the H-2I region and subdivided into I-A and I-E. H-2S includes the genes for complement components and is analogous to the “class III” region in humans. H-2T region (Qa and Tla loci) lies downstream of the main H-2 complex and contains genes for more than 25 class-I like molecules. Some function as hemopoietic differentiation molecules; others present antigens or interact with NK cells. Some of them may be pseudogenes that act as a source of DNA for gene conversion with conventional class I molecules, to promote gene diversity. Some of the genes were originally identified on thymocytes or as thymic leukemia antigens (Tla). IMMUNE RECOGNITION BY NK CELLS Natural killer cells recognize target cells that fail to express MHC class I molecules. Thus they provide a defense against viruses that attempt to evade immune recognition by downregulating MHC expression on cells they have infected. They can also recognize allogeneic cells and some tumor cells. Whether an NK cell is activated to kill the target cell depends on the balance of activating and inhibitory signals received. This allows the NK cell to interact with cells of the body and respond to changes in their MHC expression or tissue damage. Immune recognition by NK cells is complex, since some of the receptors may be expressed in both activating and inhibitory forms depending on their intracellular segments. Killer immunoglobulin-like receptors (KIRs) are a family of receptors that bind to MHC class I molecules and are used by NK cells to recognize their targets. KIRs may have two or three extracellular immunoglobulin-like domains and they are produced in two forms, an inhibitory receptor with a long cytoplasmic tail containing ITIMs (Immunoreceptor tyrosine inhibitory motifs), and an activating receptor with a short cytoplasmic tail that can interact with ITAM-containing adapter molecules. As MHC molecules have diversified, so have the KIRs that recognize them. There are several gene loci encoding KIRs (CD158). The number varies between individuals and there is much polymorphism. Each NK cell expresses a subset of the available NK-cell receptors and can therefore recognize loss or change in one group of MHC molecules. T cells may also express some KIRs after activation by antigen. LILRB1 (Leukocyte immunoglobulin-like receptor) is an inhibitory receptor expressed on monocytes, most NK cells and some T cells and B cells. It recognizes classical and nonclassical MHC class I molecules but has particularly high affinity for HLA-G, expressed only in the placenta. It therefore appears to be involved in protection of the allogeneic fetus. Lectin-like receptors are a family of receptors consisting of two polypeptides, NKG2 and CD94, which are present on most NK cells and on some cytotoxic T cells. They recognize leader peptides of MHC molecules, presented by a nonclassical MHC-encoded molecule, HLA-E. Loss of MHC molecules by a cell leads to a global reduction of MHC peptides presented by HLA-E, which can then be recognized by the NK cell or T cell. 49 NKG2 is a family of six polypeptides (NKG2A–NKG2F) which can associate with CD94 to form lectin-like receptors that recognize HLA-E, and which have either activating or inhibitory activity, depending on their cytoplasmic tail. NKG2D is an exception as it forms a homodimer, that interacts with MHC class-I-like molecules ULBP1-6 (UL-16 binding proteins) MICA and MICB. These molecules are increased in epithelia in response to heat shock, oxidative stress and viral proliferation. Hence NKG2D allows NK cells and γδ T cells to recognize tissue stress, cancerous cells and virally infected cells. Natural cytotoxicity receptors (NCRs–NKp30, NKp44, NKp46) are activating receptors on NK cells that recognize ligands expressed on cancerous and virally infected cells and changes in surface properties of those cells. They work in association with an adhesion molecule DNAM-1, which is also present on most T cells, macrophages and dendritic cells. NK cell receptors ligands INHIBITORY INHIBITORY ITIMs ITIMs CD94 NKG2A ACTIVATING CD94 NKG2C ACTIVATING NKG2D NKG2D LILR1B MHC leader peptide HLA-E HLA-A/B/C HLA-G Fig. 2.19 NK cell lectin-like receptors and LL1R1B.







1.4 Major histocompatibility complex MHC is a family of genes present in most of the vertebrates. The MHC consists of large portion of DNA covering about 4 million base pairs in humans or about 0.1% of human genome, and has over 200 coding loci (Caroline & Campbell, 2001). In mice MHC cluster is present on chromosome 17. In humans, chromosome 6 has a locus which consists of three subfamilies clustered near each other, in between MHC class I and II is present class III. Immunological self/nonself is influenced by MHC class I and II genes, which are highly polymorphic loci known in vertebrates. Glycoproteins encoded by class I are present on the exterior of all the nucleated somatic cells, while MHC class II glycoproteins are a part of specialized antigen presenting cells (APCs), such as dendritic cells, macrophages, and B cells. MHC class I molecules are responsible for the presentation of peptide (antigen) which are intrinsic to CD81 cytotoxic T lymphocytes (CTLs). As far as MHC class II are concerned, they are responsible for the presentation of peptide (antigen) which are extrinsic to CD41 helper T (TH) cells. Both cell and antibody mediated specific immunological responses are controlled by MHC through antigen presentation. MHC were discovered due to their fascinating role in tissue transplantation, but today of all the genetic systems, MHC genes are exhaustively studied as they control the crucial traits, including resistance to infectious diseases. After the discovery of MHC, it almost took 20 long years to understand its biological role in peptide presentation and its response to T cells. The main task of T cells is to protect the body against any invasion and to activate the macrophages and B lymphocytes. For this activation T cells need to interact with different cells like infected host cells, macrophages, dendritic cells, and B lymphocytes. T cells can recognize the antigen presented on other cells while as B cell receptor can recognize the antigens presented on cell surface. These cellular antigens are presented on protein molecules that are encoded by genes in a locus called MHC. The genes in these loci determine the fate of the tissue transplant based on the compatibility of genetic loci of the two individuals. The main feature of MHC loci is that it is polymorphic having alternate forms of genes. (Kim, Jennifer, et al., 2005) 1.5 MHC class I Glycoproteins called MHC molecules are expressed on almost all nucleated cells by MHC class I. Each MHC class I codes for a 43 kDa transmembrane glycoprotein referred to as alpha or heavy chain. Each heavy chain consists of three extracellular domains: alpha 1, alpha 2, and alpha 3. It is the alpha 3 which is highly conserved and interacts with CD8 molecule present on cytotoxic T cells. The expression of MHC class I is possible only in association with small molecule called Beta 2 microglobulin, which is 12 kDa invariant polypeptide (Table 1.1). Class I are manifested on all the nucleated cells, though the expression varies, the highest being expressed by lymphocytes while hepatocytes express them at a very low level. (Somak, 2020) (Fig. 1.2) 1.6 MHC class II Like MHC class I, class II MHC is transmembrane glycoprotein molecules with cytoplasmic tail and extracellular like domains which are called as alpha 1, alpha 2, beta 1, and beta 2. Class II MHC genes codes for alpha and Beta chains of approximately molecular weight 35,000 and 28,000 Da, 1.7 MHC class III This class include all the genes that are associated with components of complement are also coding for various proteins involved in immune response. Antigen presentation is mediated by T cell receptors. These T cells recognize the antigen only when it is combined with MHC molecules. Both helper and cytotoxic T cells require MHC molecules for antigen presentation. This process is called as self MHC restriction Class I present processed endogenous antigen to CD8 T cells while class II present it to CD4 T cells. Both exogenous and endogenous antigens are processes differently. (Gruen & Weisman, 2001) system, factors related to inflammation. Besides this class of genes

The MHC loci on chromosome 6 is a crucial predisposing factor for number of auto immune diseases (Vasiliki, Vinod, et al., 2017).


A potential example of disassortative mating in humans is the major histocompatibility complex (MHC) (Laurent and Chaix, 2012a,b). MHC is a genomic region containing multiple genes coding for molecules whose role is to present self- and non self-derived peptide antigens to T cells, thereby playing a critical role in immune response and in organ transplant success. MHC is a 3.6 mega base pair long region located on the short arm of chromosome 6 in the human genome. Many of these same MHC genes influence body odor, and studies in other species and possibly humans indicate disassortative mating at MHC mediated by olfactory cues (Havlicek and Roberts, 2009). As expected for

a region under disassortative mating, the MHC region shows a significantly higher level of heterozygosity

<"The possible adaptive advantages are clear: it is a mechanism of avoiding inbreeding and MHC-heterozygous offspring may have enhanced immunocompetence."

than other regions of the human genome (Laurent and Chaix, 2012b). However, many studies do not indicate disassortative mating at MHC, and a meta analysis of MHC effects on human mating revealed both MHC-dissimilar and MHC-similar matings in various studies (Winternitz et al., 2017). This seemingly contradictory pattern appears to be an artifact of population ethnic heterogeneity in observational studies that tend to indicate assortative mating versus experimental studies with more control over sociocultural biases that tend to indicate disassortative mating or mating for diverse MHC mates (Winternitz et al., 2017). In many areas of the world, human populations from diverse

geographical areas and with different cultures have been brought together, as will be discussed in detail

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The simplest system of mating is random mating in which individuals choose mates at random and independently of the genotypes of interest; that is, the probability of two genotypes being mates is simply the product of the frequencies of the two genotypes in the deme. The implications of this system of mating were modeled by Wilhelm Weinberg (1908), a German physician interested in Mendelian inheritance in humans, and Geoffrey Hardy (1908), an English mathematician who was addressing the issue of the

frequency of a Mendelian trait in a human population versus Mendelian ratios in a particular family. Despite the simplicity of the model they independently developed, it was and remains a cornerstone of population genetic theory. Both modeled a single autosomal locus with two alleles, say A and a, with no mutation, subject to the simplifying assumptions stated above and with all genotypes having equal

viability, mating success, and fertility (no natural selection). In addition, Weinberg assumed that all frequencies were identical in males and females, and Hardy assumed that all individuals were self-compatible hermaphrodites that were as likely to mate with themselves as any other individual in the deme. Weinberg used a family model to derive what is now known as the Hardy Weinberg Law (Table 3.1). His model assumes that the initial genotype frequencies (the same in both sexes) are GAA for genotype AA, GAa for Aa, and Gaa for aa. Table 3.1 shows all possible mating types from these three genotypes, with the convention of putting the female first and the male second. The frequency of the

mating pair is simply the product of the respective genotype frequencies, as shown in Table 3.1. Mendel’s first law is then used to calculate the probabilities of each type of offspring arising from each type of mating pair (Table 3.1). To obtain the next generation’s genotype frequencies, say G0ij where i and j can be either A or a, Weinberg multiplied the Mendelian probability of a specific genotype from a specific mating type times the probability of the mating type under random mating, and then took the

sum over all possible mating types for each offspring genotype.

ree

As can be seen from Table 3.7, this system of mating produces many heterozygotes and few homozygotes-just the opposite of assortative mating. For example, suppose we started out with Hardy-Weinberg genotype frequencies with p ¼ 0.25, with an initial heterozygote frequency of 0.375. Then in a single generation of disassortative mating as given by Table 3.7, the frequency of heterozygotes would increase to 0.565. Unlike the assortative mating model, in this case the allele frequency also changes from 0.25 to 0.326, so disassortative mating is a strong evolutionary force at the single locus level. However, with p ¼ 0.326, the expected heterozygosity under random mating is 0.439, so there is still a heterozygous excess under disassortative mating with f¼0.286. Hence, disassortative mating resembles avoidance of inbreeding, but unlike avoidance of inbreeding, it only affects the loci contributing to the phenotype for which disassortative mating is occurring and loci in linkage disequilibrium with them. In addition, unlike avoidance of inbreeding, disassortative mating alters allele frequencies and tends to stabilize them at intermediate levels. At the multi-locus level, disassortative mating can bring together into the same family alleles that have opposite effects on phenotypes. This could potentially generate some linkage disequilibrium, but by also causing excesses of heterozygosity, disassortative mating dissipates linkage disequilibrium much more rapidly than random mating (recall, recombination only changes gamete frequencies in double heterozygotes). Hence, disassortative mating is not as effective as assortative mating in generating or maintaining linkage disequilibrium.


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Molecular phylogenies map to biogeography better than morphological ones

"Tiger Salamander"

The term “species complex,” while not a formal taxonomic category, is often used to describe groups of closely related lineages, sometimes arising through a burst of diversification. The tiger salamander species complex has been highlighted as a potentially valuable example of such a recent and rapid radiation (15) that could provide insight into the early mechanisms initiating and/or maintaining diversity.

Bingo, Genetic Diversity!

paedomorphosis?







 
 
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