“…ICAM-1) in order to protect from cerebral malaria. 80,81 The rapid non-synonymous evolution of CD36 genes driven by positive selection in human or in primates could not only be related to the multiple-function divergence of CD36, but also to multiple malaria parasitism with host shift through Plasmodium evolution. 8–11 Figure 3.Posterior probability of the inferred positively selected sites estimated from site models of M2a and M8.…”
Plasmodium-induced malaria widely infects primates and other mammals. Multiple past studies have revealed that positive selection could be the main evolutionary force triggering the genetic diversity of anti-malaria resistance-associated genes in human or primates. However, researchers focused most of their attention on the infra-generic and intra-specific genome evolution rather than analyzing the complete evolutionary history of mammals. Here we extend previous research by testing the evolutionary link of natural selection on eight candidate genes associated with malaria resistance in mammals. Three of the eight genes were detected to be affected by recombination, including TNF-α, iNOS and DARC. Positive selection was detected in the rest five immunogenes multiple times in different ancestral lineages of extant species throughout the mammalian evolution. Signals of positive selection were exposed in four malaria-related immunogenes in primates: CCL2, IL-10, HO1 and CD36. However, selection signals of G6PD have only been detected in non-primate eutherians. Significantly higher evolutionary rates and more radical amino acid replacement were also detected in primate CD36, suggesting its functional divergence from other eutherians. Prevalent positive selection throughout the evolutionary trajectory of mammalian malaria-related genes supports the arms race evolutionary hypothesis of host genetic response of mammalian immunogenes to infectious pathogens.
“…ICAM-1) in order to protect from cerebral malaria. 80,81 The rapid non-synonymous evolution of CD36 genes driven by positive selection in human or in primates could not only be related to the multiple-function divergence of CD36, but also to multiple malaria parasitism with host shift through Plasmodium evolution. 8–11 Figure 3.Posterior probability of the inferred positively selected sites estimated from site models of M2a and M8.…”
Plasmodium-induced malaria widely infects primates and other mammals. Multiple past studies have revealed that positive selection could be the main evolutionary force triggering the genetic diversity of anti-malaria resistance-associated genes in human or primates. However, researchers focused most of their attention on the infra-generic and intra-specific genome evolution rather than analyzing the complete evolutionary history of mammals. Here we extend previous research by testing the evolutionary link of natural selection on eight candidate genes associated with malaria resistance in mammals. Three of the eight genes were detected to be affected by recombination, including TNF-α, iNOS and DARC. Positive selection was detected in the rest five immunogenes multiple times in different ancestral lineages of extant species throughout the mammalian evolution. Signals of positive selection were exposed in four malaria-related immunogenes in primates: CCL2, IL-10, HO1 and CD36. However, selection signals of G6PD have only been detected in non-primate eutherians. Significantly higher evolutionary rates and more radical amino acid replacement were also detected in primate CD36, suggesting its functional divergence from other eutherians. Prevalent positive selection throughout the evolutionary trajectory of mammalian malaria-related genes supports the arms race evolutionary hypothesis of host genetic response of mammalian immunogenes to infectious pathogens.
“…Previous data have suggested that parasitic diseases may drive host diversification when non-interbreeding host populations evolve different mechanisms for disease resistance [ 42 , 43 , 44 ]. For example, human exposure to the malaria parasite Plasmodium falciparum approximately 10,000 years ago led to different genetically based mechanisms of malaria resistance in geographically isolated locations, including haemoglobin S in sub-Saharan Africa, beta-thalassemia in the Mediterranean and ovalocytosis in Southeast Asia [ 43 , 45 , 46 , 47 ]. In a similar manner, exposure of the LCA to tick-borne diseases in geographically isolated host populations may have driven selection for hair loss in humans [ 32 , 36 ] and grooming behaviour in chimpanzees [ 35 , 48 , 49 ] as evolutionarily divergent anti-tick strategies.…”
Human straight-legged bipedalism represents one of the earliest events in the evolutionary split between humans (Homo spp.) and chimpanzees (Pan spp.), although its selective basis is a mystery. A carrying-related hypothesis has recently been proposed in which hair loss within the hominin lineage resulted in the inability of babies to cling to their mothers, requiring mothers to walk upright to carry their babies. However, a question remains for this model: what drove the hair loss that resulted in upright walking? Observers since Darwin have suggested that hair loss in humans may represent an evolutionary strategy for defence against ticks. The aim of this review is to propose and evaluate a novel tick-based evolutionary hypothesis wherein forest fragmentation in hominin paleoenvironments created conditions that were favourable for tick proliferation, selecting for hair loss in hominins and grooming behaviour in chimpanzees as divergent anti-tick strategies. It is argued that these divergent anti-tick strategies resulted in different methods for carrying babies, driving the locomotor divergence of humans and chimpanzees.
Brazilian quilombos are communities formed by enslaved Africans and their descendants all over the country during slavery and shortly after its abolition. Quilombos harbor a great fraction of the largely unknown genetic diversity of the African diaspora in Brazil. Thus, genetic studies in quilombos have the potential to provide important insights not only into the African roots of the Brazilian population but also into the genetic bases of complex traits and human adaptation to diverse environments. This review summarizes the main results of genetic studies performed on quilombos so far. Here, we analyzed the patterns of African, Amerindian, European, and subcontinental ancestry (within Africa) of quilombos from the five different geographic regions of Brazil. In addition, uniparental markers (from the mtDNA and the Y chromosome) studies are analyzed together to reveal demographic processes and sex-biased admixture that occurred during the formation of these unique populations. Lastly, the prevalence of known malaria-adaptive African mutations and other African-specific variants discovered in quilombos, as well as the genetic bases of health-related traits, are discussed here, together with their implication for the health of populations of African descent.
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