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Africa
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Pretty People / Aesthetic Enhancement
Published in Jonathan Anomaly, Creating Future People, 2020
By contrast, facial symmetry, which is aesthetically desired by both men and women, may be an honest signal of a low mutation load, low oxidative stress, or a low parasite load. Mutations accumulate every generation and, in the absence of purifying selection, can add up to significant fitness costs.3 Indeed, according to Geoffrey Miller, ‘sexual reproduction probably arose as a way to contain the damage caused by mutations’ (2000, p. 101). William Hamilton proposed (and Miller agrees) that sexual reproduction evolved at least in part as a defense against parasites, so that by shuffling the genetic deck every generation our immune system can keep up with the evolution of deadly microbes (Hamilton et al., 1990). And a number of authors have traced facial asymmetry and premature aging to the oxidative stress that occurs when free radicals escape during cellular metabolism (Lane, 2004). If any of these theories are true, traits we find beautiful are to some extent an indicator of genetic health.4
Laboratory Studies
Published in Jacques Derek Charlwood, The Ecology of Malaria Vectors, 2019
A large amount of nucleotide variation has been shown to exist in genes when they are sampled from natural populations. Each novel nucleotide sequence is considered a novel allele. Variation among alleles consists primarily of synonymous substitutions that do not change the primary amino acid sequence. The majority of non-synonymous substitutions involve changes among amino acids of similar size, function or charge. This pattern of variation is consistent with the neutral theory of molecular evolution. This model assumes that most mutations are deleterious to the fitness of an individual and are removed through purifying selection.
Motoo Kimura (1924–1994)
Published in Krishna Dronamraju, A Century of Geneticists, 2018
Neutral theory does not deny the occurrence of natural selection. There are two main types of natural selection: stabilizing selection or purifying selection, which acts to eliminate deleterious mutations; and positive selection, which favors advantageous mutations.
Searching for archaic contribution in Africa
Published in Annals of Human Biology, 2019
Cindy Santander, Francesco Montinaro, Cristian Capelli
Recent studies looking at African hunter-gatherer and farmer populations have explored how deleterious genetic variation amongst human populations is affected by changes in population size and gene flow (Lopez et al. 2018). Specifically, hunter-gatherers are efficient in purifying selection, despite having a recent population collapse (Simons et al. 2014; Lopez et al. 2018). Long-term selection against archaic introgression in Africa has not been looked at, although recent studies have shown that non-African populations demonstrate selection against introgression in regulatory regions more than in protein-coding regions (Petr et al. 2019). A study exploring the genetic relationship between sequenced archaic hominins and Africans showed substantial IBD sharing between Africans (East and West) and Denisovans best explained by interbreeding between the ancestor of humans and other archaic hominins (Povysil and Hochreiter 2016). Whether these short IBD fragments are skewed in their distribution across genic and non-genic regions remains to be confirmed as well if they are putatively introgressed haplotypes under any form of non-neutral selection. However, Durvasula and Sankararaman (2018) have detected a number of regions with archaic ancestry in Yoruba which are in genic regions and that may be under positive selection (Table 1). Nevertheless, it is important to point out that without ancient African samples to confirm archaic introgression in present-day African populations, signs of adaptive introgression will remain putative.
Diversifying selection detected in only a minority of xenobiotic-metabolizing CYP1-3 genes among primate species
Published in Xenobiotica, 2020
Morgan E. Chaney, Melia G. Romine, Helen Piontkivska, Anthony J. Tosi
Though our prediction related to P450 copy-number variation was not supported by a null-hypothesis significance test, we believe that this question is worth repeating with other taxonomic groups, especially within species, because there are case examples in which expansion or contraction of specific subfamilies have been dramatic and adaptive (e.g., Johnson et al., 2018). On the other hand, from the results reported here, we would expect any increases in variance between EM and XM subfamilies to be driven as much by gene loss as by gene birth. In cases where a species is highly specialized on a diet that does not require the detoxification of certain toxic compounds, purifying selection may act on related P450 genes to the point where those genes not only become pseudogenized but may become highly prevalent in the population or even reach fixity. Thus, the loss of a gene would be a significant event and would likely form a significant limit on the evolution of that lineage (Sharma et al., 2018). To follow up the findings presented here, instances where a subfamily was found to be absent should be tested with population-genetic datasets containing multiple individuals because many of the primate genomes on NCBI are derived from a single animal of a given species. This would be necessary in parsing polymorphic copy number variants from divergent copy number differences, particularly in light of subfamilies known to be polymorphic in humans or other primates (e.g., CYP2D: Ingelman-Sundberg, 2005). Such work stands to inform not only the population genetics of a species but also microevolutionary adaptation to local environments (e.g., see Osada et al., 2010). In this way, the study of P450s among populations represents a valuable avenue for future work by population geneticists.
Taishan Pinus massoniana Pollen Polysaccharides Enhance Immune Responses in Chickens Infected by Avian Leukosis Virus Subgroup B
Published in Immunological Investigations, 2018
Shifa Yang, Guiming Li, Zengcheng Zhao, Zhongli Huang, Jian Fu, Minxun Song, Shuqian Lin, Ruiliang Zhu
Immunosuppressive diseases in chickens can be caused by various pathogens such as viruses, bacteria, and fungi, which result in diminished immunity and antibody levels. Immunosuppression destroys the immune system of chickens and makes them more vulnerable to pathogens, leading to severe economic losses in poultry industry during rearing (Zhou et al., 2011). Immunosuppressive diseases could also cause secondary infection and mixed infection in chicken flocks (Hoerr, 2010). Previous studies have reported that several avian immunosuppressive viruses, such as avian leukemia virus (ALV), avian reticuloendotheliosis virus, and Marek’s disease virus, can induce immunosuppression in chickens and increase their susceptibility to other pathogens (Feng et al., 2016; Neerukonda et al., 2016; Puro et al., 2015). ALV has been detected in chicken flocks in recent years and spread widely in the world. ALV is a type C retrovirus, contributing a variety of neoplasms including lymphoid and myeloid leukosis. ALV can be divided into subgroups A-J according to the nucleotide sequences of its gp85 protein (Du Yan et al., 2000). Although ALV-J was the predominant pandemic strain in China, ALV-B epidemic has also been reported during the last few years (Duan et al., 2014; Shu-Zhen et al., 2016). Compared to ALV-J, ALV-B shows relatively prevalence and mortality rate and often induces immunosuppression instead of causing death in chicken. Chickens infected by ALV-B exhibit decreased weight loss, egg production, and breeding potential (Feng et al., 2011; Gavora et al., 1980). Generally, the immunosuppressive virus is difficult to control because it usually exists via latent infection. To date, ALV-B vaccines or drugs have not been developed. Currently, purifying selection is the most effective strategy for ALV-B prevention; however, the process is time-consuming and expensive. Therefore, it is essential to develop a therapeutic method to improve the immune functions of chickens infected with ALV-B.