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Genetic admixture is central to primate evolution. We combined 50 years of field observations of immigration and group demography with genomic data from ~9 generations of hybrid baboons to investigate the consequences of admixture in the wild. Despite no obvious fitness costs to hybrids, we found signatures of selection against admixture similar to those described for archaic hominins. These patterns were concentrated near genes where ancestry is strongly associated with gene expression. Our analyses also show that introgression is partially predictable across the genome. This study demonstrates the value of integrating genomic and field data for revealing how “genomic signatures of selection” (e.g., reduced introgression in low-recombination regions) manifest in nature; moreover, it underscores the importance of other primates as living models for human evolution. 

Experiences early in life can have lasting effects on the health and survival of humans and other creatures. Whether early hardships can also influence the wellbeing of the next generation is less clear. One previous study with captive hamsters suggested that adversity early in the life of a mother may indeed shorten how long her offspring will live. But hamsters only live for a few years and much less is known about the possibility for intergenerational effects in animals with longer lifespans. This is partly because such studies are time-consuming and thus more difficult to complete. Over the past 45 years, scientists have collected data on generations of baboons living in and around the Amboseli National Park in southern Kenya. Baboons live in social groups with a strict hierarchy, and individuals can live for up to 30 years in the wild. Previous research has shown that early life adversity – such as being orphaned or simply having a low-ranking mother – can shorten the lifespan of female baboons even if they make it to adulthood. It was unclear, however, whether these ill effects could be passed on to the next generation. Now, Zipple et al. have used the wealth of data about the Amboseli baboons to find the answer. After taking into account any adversity that each baboon experienced directly, Zipple et al. showed that juvenile baboons whose mothers were orphaned before reaching adulthood were 44% more likely to die young than juveniles whose grandmothers survived during their mother’s early years. Baboons whose mothers had a close-in-age younger sibling were also 42% more likely to die early as compared to those whose mothers did not, perhaps because the younger sibling competed with the mother for access to maternal care. The analysis suggests that early life adversity in female baboons can have intergenerational effects. More studies are needed to determine if this is also true of humans. If it is, such a result may help explain the persistence of poor health outcomes across generations and shed light on how best to intervene to interrupt this transmission. 

Abstract Is it possible to slow the rate of ageing, or do biological constraints limit its plasticity? We test the ‘invariant rate of ageing’ hypothesis, which posits that the rate of ageing is relatively fixed within species, with a collection of 39 human and nonhuman primate datasets across seven genera. We first recapitulate, in nonhuman primates, the highly regular relationship between life expectancy and lifespan equality seen in humans. We next demonstrate that variation in the rate of ageing within genera is orders of magnitude smaller than variation in pre-adult and age-independent mortality. Finally, we demonstrate that changes in the rate of ageing, but not other mortality parameters, produce striking, species-atypical changes in mortality patterns. Our results support the invariant rate of ageing hypothesis, implying biological constraints on how much the human rate of ageing can be slowed. 

Abstract ObjectivesPregnancy failure represents a major fitness cost for any mammal, particularly those with slow life histories such as primates. Here, we quantified the risk of fetal loss in wild hybrid baboons, including genetic, ecological, and demographic sources of variance. We were particularly interested in testing the hypothesis that hybridization increases fetal loss rates. Such an effect would help explain how baboons may maintain genetic and phenotypic integrity despite interspecific gene flow. Materials and MethodsWe analyzed outcomes for 1020 pregnancies observed over 46 years in a natural yellow baboon‐anubis baboon hybrid zone. Fetal losses and live births were scored based on records of female reproductive state and the appearance of live neonates. We modeled the probability of fetal loss as a function of a female's genetic ancestry (the proportion of her genome estimated to be descended from anubis [vs. yellow] ancestors), age, number of previous fetal losses, dominance rank, group size, climate, and habitat quality using binomial mixed effects models. ResultsFemale genetic ancestry did not predict fetal loss. Instead, the risk of fetal loss is elevated for very young and very old females. Fetal loss is most robustly predicted by ecological factors, including poor habitat quality prior to a home range shift and extreme heat during pregnancy. DiscussionOur results suggest that gene flow between yellow and anubis baboons is not impeded by an increased risk of fetal loss for hybrid females. Instead, ecological conditions and female age are key determinants of this component of female reproductive success. 

Relatives have more similar gut microbiomes than nonrelatives, but the degree to which this similarity results from shared genotypes versus shared environments has been controversial. Here, we leveraged 16,234 gut microbiome profiles, collected over 14 years from 585 wild baboons, to reveal that host genetic effects on the gut microbiome are nearly universal. Controlling for diet, age, and socioecological variation, 97% of microbiome phenotypes were significantly heritable, including several reported as heritable in humans. Heritability was typically low (mean = 0.068) but was systematically greater in the dry season, with low diet diversity, and in older hosts. We show that longitudinal profiles and large sample sizes are crucial to quantifying microbiome heritability, and indicate scope for selection on microbiome characteristics as a host phenotype.