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Szpiech, Z. A.

Publications and source records attributed to Szpiech, Z. A..

25 records · Page 2Linked to original sources

High-altitude adaptation in rhesus macaques

When natural populations split and migrate to different environments, they may experience different selection pressures that can lead to local adaptation. To capture the genomic patterns of a local selective sweep, we develop XP-nSL, a genomic scan for local adaptation that compares haplotype patterns between two populations. We show that XP-nSL has power to detect ongoing and recently completed hard and soft sweeps, and we then apply this statistic to search for evidence of adaptation to high altitude in rhesus macaques. We analyze the whole genomes of 23 wild rhesus macaques captured at high altitude (mean altitude > 4000m above sea level) to 22 wild rhesus macaques captured at low altitude (mean altitude < 500m above sea level) and find evidence of local adaptation in the high-altitude population at or near 303 known genes and several unannotated regions. We find the strongest signal for adaptation at EGLN1, a classic target for convergent evolution in several species living in low oxygen environments. Furthermore, many of the 303 genes are involved in processes related to hypoxia, regulation of ROS, DNA damage repair, synaptic signaling, and metabolism. These results suggest that, beyond adapting via a beneficial mutation in one single gene, adaptation to high altitude in rhesus macaques is polygenic and spread across numerous important biological systems. Impact SummaryWhen positive selection is ongoing or a beneficial mutation has recently fixed in a population, genetic diversity is reduced in the vicinity of the adaptive allele, and we expect to observe long homozygous haplotypes at high frequency. Here we develop a statistic that summarizes these expected patterns and compares between two populations in order to search for evidence of adaptation that may have occurred in one but not the other. We implement this statistic in a popular and easy-to-use software package, and then apply it to study adaptation to high altitude in rhesus macaques. Extreme environments pose a challenge to life on multiple fronts. Very high-altitude environments are one such example, with low atmospheric oxygen, increased ultraviolet light exposure, harsh temperatures, and reduced nutrition availability. In spite of these challenges, many plants and animals, including humans, have genetically adapted to cope with these hardships. Here we study two populations of rhesus macaques, one living at high altitude and one living close to sea level. We apply our novel statistic to compare their haplotype patterns between them to search for evidence of genetic changes that are indicative of adaptation to their environment. We find evidence for adaptation at a critical gene that helps control physiological response to low-oxygen, one that has been the target of repeated convergent evolution across many species. We also find evidence for positive selection across a range of traits, including metabolic and neurological. This work helps to explain the evolutionary history of the rhesus macaque and furthers our understanding about the ways organisms genetically adapt to high-altitude environments.

evolutionary biology↗

The bear bones: mosaic ancestry of Macaca arctoides explains divergent baculum morphology

Genital divergence is thought to contribute to reproductive barriers by establishing a "lock- and-key" mechanism for reproductive compatibility. One such example, Macaca arctoides, the bear macaque, has compensatory changes in both male and female genital morphology as compared to close relatives. Macaca arctoides also has a complex evolutionary history, having extensive introgression between the fascicularis and sinica macaque species groups. Here, phylogenetic relationships were analyzed via whole genome sequences from five species, including M. arctoides, and two species each from the putative parental species groups. This analysis revealed [~]3x more genomic regions supported placement in the sinica species group as compared to the fascicularis species group. Additionally, introgression analysis of the M. arctoides genome revealed it is a mosaic of recent polymorphisms shared with both species groups. To examine the evolution of their unique genital morphology further, the prevalence of candidate genes involved in genital morphology were compared against genome-wide outliers in various population genetic metrics, while accounting for background variation in recombination rate. This analysis identified 66 outlier genes, including several genes that influence baculum morphology in mice, which were of interest since the bear macaque has the longest primate baculum. The mean of several metrics was statistically different in the candidate genes as compared to the rest of the genome, suggesting that genes involved in genital morphology have increased divergence and decreased diversity beyond expectations. These results highlight how extensive introgression may have contributed to reproductive isolation and shaped the unique genital morphology in the bear macaque.

evolutionary biology↗

Sequencing of 53,831 diverse genomes from the NHLBI TOPMed Program

Summary paragraphThe Trans-Omics for Precision Medicine (TOPMed) program seeks to elucidate the genetic architecture and disease biology of heart, lung, blood, and sleep disorders, with the ultimate goal of improving diagnosis, treatment, and prevention. The initial phases of the program focus on whole genome sequencing of individuals with rich phenotypic data and diverse backgrounds. Here, we describe TOPMed goals and design as well as resources and early insights from the sequence data. The resources include a variant browser, a genotype imputation panel, and sharing of genomic and phenotypic data via dbGaP. In 53,581 TOPMed samples, >400 million single-nucleotide and insertion/deletion variants were detected by alignment with the reference genome. Additional novel variants are detectable through assembly of unmapped reads and customized analysis in highly variable loci. Among the >400 million variants detected, 97% have frequency <1% and 46% are singletons. These rare variants provide insights into mutational processes and recent human evolutionary history. The nearly complete catalog of genetic variation in TOPMed studies provides unique opportunities for exploring the contributions of rare and non-coding sequence variants to phenotypic variation. Furthermore, combining TOPMed haplotypes with modern imputation methods improves the power and extends the reach of nearly all genome-wide association studies to include variants down to ~0.01% in frequency.

genomics↗

Ancestry-dependent Enrichment of Deleterious Homozygotes in Runs of Homozygosity

Runs of homozygosity (ROH) are important genomic features that manifest when an individual inherits two haplotypes that are identical-by-descent. Their length distributions are informative about population history, and their genomic locations are useful for mapping recessive loci contributing to both Mendelian and complex disease risk. We have previously shown that ROH, and especially long ROH that are likely the result of recent parental relatedness, are enriched for homozygous deleterious coding variation in a worldwide sample of outbred individuals. However, the distribution of ROH in admixed populations and their relationship to deleterious homozygous genotypes is understudied. Here we analyze whole genome sequencing data from 1,441 individuals from self-identified African American, Puerto Rican, and Mexican American populations. These populations are three-way admixed between European, African, and Native American ancestries and provide an opportunity to study the distribution of deleterious alleles partitioned by local ancestry and ROH. We re-capitulate previous findings that long ROH are enriched for deleterious variation genome-wide. We then partition by local ancestry and show that deleterious homozygotes arise at a higher rate when ROH overlap African ancestry segments than when they overlap European or Native American ancestry segments of the genome. These results suggest that, while ROH on any haplotype background are associated with an inflation of deleterious homozygous variation, African haplotype backgrounds may play a particularly important role in the genetic architecture of complex diseases for admixed individuals, highlighting the need for further study of these populations.

genetics↗

Human demographic history has amplified the effects background selection across the genome

Natural populations often grow, shrink, and migrate over time. Demographic processes such as these can impact genome-wide levels of genetic diversity. In addition, genetic variation in functional regions of the genome can be altered by natural selection, which drives adaptive mutations to higher frequencies or purges deleterious ones. Such selective processes impact not only the sites directly under selection but also nearby neutral variation through genetic linkage through processes referred to as genetic hitch-hiking in the context of positive selection and background selection (BGS) in the context of purifying selection. While there is extensive literature examining the impact of selection at linked sites at demographic equilibrium, less is known about how non-equilibrium demographic processes impact the effects of hitchhiking and BGS. Utilizing a global sample of human whole-genome sequences from the Thousand Genomes Project and extensive simulations, we investigate how non-equilibrium demographic processes magnify and dampen the consequences of selection at linked sites across the human genome. When binning the genome by inferred strength of BGS, we observe that, compared to Africans, non-African populations have experienced larger proportional decreases in neutral genetic diversity in such regions. We replicate these findings in admixed populations by showing that non-African ancestral components of the genome have also been impacted more severely in these regions. We attribute these differences to the strong, sustained/recurrent population bottlenecks that non-Africans experienced as they migrated out of Africa and throughout the globe. Furthermore, we observe a strong correlation between FST and inferred strength of BGS, suggesting a stronger rate of genetic drift. Forward simulations of human demographic history with a model of BGS support these observations. Our results show that non-equilibrium demography significantly alters the consequences selection at linked sites and support the need for more work investigating the dynamic process of multiple evolutionary forces operating in concert.\n\nAuthor summaryPatterns of genetic diversity within a species are affected at broad and fine scales by population size changes (\"demography\") and natural selection. From both population genetics theory and observation of genomic sequence data, it is known that demography can alter genome-wide average neutral genetic diversity. Additionally, natural selection can affect neutral genetic diversity regionally across the genome via selection at linked sites. During this process, natural selection acting on adaptive or deleterious variants in the genome will also impact diversity at nearby neutral sites due to genetic linkage. However, less is well known about the dynamic changes to diversity that occur in regions impacted by selection at linked sites when a population undergoes a size change. We characterize these dynamic changes using thousands of human genomes and find that the population size changes experienced by humans have shaped the consequences of linked selection across the genome. In particular, population contractions, such as those experienced by non-Africans, have disproportionately decreased neutral diversity in regions of the genome inferred to be under strong background selection (i.e., selection at linked sites that is caused by natural selection acting on deleterious variants), resulting in large differences between African and non-African populations.

evolutionary biology↗

Prominent Features Of The Amino Acid Mutation Landscape In Cancer

Cancer can be viewed as a set of different diseases with distinctions based on tissue origin, driver mutations, and genetic signatures. Accordingly, each of these distinctions have been used to classify cancer subtypes and to reveal common features. Here, we present a different analysis of cancer based on amino acid mutation signatures. Non-negative Matrix Factorization and principal component analysis of 29 cancers revealed six amino acid mutation signatures, including four signatures that were dominated by either arginine to histidine (Arg>His) or glutamate to lysine (Glu>Lys) mutations. Sample-level analyses reveal that while some cancers are heterogeneous, others are largely dominated by one type of mutation. Using a non-overlapping set of samples from the COSMIC somatic mutation database, we validate five of six mutation signatures, including signatures with prominent arginine to histidine (Arg>His) or glutamate to lysine (Glu>Lys) mutations. This suggests that our classification of cancers based on amino acid mutation patterns may provide avenues of inquiry pertaining to specific protein mutations that may generate novel insights into cancer biology.

bioinformatics↗

Whole Genome Sequencing of Pharmacogenetic Drug Response in Racially and Ethnically Diverse Children with Asthma

Asthma is the most common chronic disease of children, with significant racial/ethnic differences in prevalence, morbidity, mortality and therapeutic response. Albuterol, a bronchodilator medication, is the first-line therapy for asthma treatment worldwide. We performed the largest whole genome sequencing (WGS) pharmacogenetics study to date using data from 1,441 minority children with asthma who had extremely high or low bronchodilator drug response (BDR). We identified population-specific and shared pharmacogenetic variants associated with BDR, including genome-wide significant (p < 3.53 x 10-7) and suggestive (p < 7.06 x 10-6) loci near genes previously associated with lung capacity (DNAH5), immunity (NFKB1 and PLCB1), and {beta}-adrenergic signaling pathways (ADAMTS3 and COX18). Functional analyses centered on NFKB1 revealed potential regulatory function of our BDR-associated SNPs in bronchial smooth muscle cells. Specifically, these variants are in linkage disequilibrium with SNPs in a functionally active enhancer, and are also expression quantitative trait loci (eQTL) for a neighboring gene, SLC39A8. Given the lack of other asthma study populations with WGS data on minority children, replication of our rare variant associations is infeasible. We attempted to replicate our common variant findings in five independent studies with GWAS data. The age-specific associations previously found in asthma and asthma-related traits suggest that the over-representation of adults in our replication populations may have contributed to our lack of statistical replication, despite the functional relevance of the NFKB1 variants demonstrated by our functional assays. Our study expands the understanding of pharmacogenetic analyses in racially/ethnically diverse populations and advances the foundation for precision medicine in at-risk and understudied minority populations.\n\nAUTHOR SUMMARYAsthma is the most common chronic disease among children. Albuterol, a bronchodilator medication, is the first-line therapy for asthma treatment worldwide. In the U.S., asthma prevalence is the highest among Puerto Ricans, intermediate among African Americans and lowest in Whites and Mexicans. Asthma disparities extend to mortality, which is four- to five-fold higher in Puerto Ricans and African Americans compared to Mexicans [1]. Puerto Ricans and African Americans, the populations with the highest asthma prevalence and death rate, also have the lowest albuterol bronchodilator drug response (BDR). We conducted the largest pharmacogenetic study using whole genome sequencing data from 1,441 minority children with asthma who had extremely high or low albuterol bronchodilator drug response. We identified population-specific and shared pharmacogenetic variants associated with BDR. Our findings help inform the direction of future development of asthma medications and our study advances the foundation of precision medicine for at-risk, yet understudied, racially/ethnically diverse populations.

genetics↗