bioRxiv ScienceSearch

bioRxiv · 10.1101/2021.05.24.445417

Signatures of genetic variation in human microRNAs point to processes of positive selection related to population-specific disease risks

Abstract

The occurrence of natural variation in human microRNAs has been the focus of numerous studies during the last twenty years. Most of them have been dedicated to study the role of specific mutations in diseases, like cancer, while a minor fraction seek to analyse the diversity profiles of microRNAs in the genomes of human populations. In the present study we analyse the latest human microRNA annotations in the light of the most updated catalog of genetic variation provided by the 1000 Genomes Project. We show by means of the in silico analysis of noncoding variation of microRNAs that the level of evolutionary constraint of these sequences is governed by the interplay of different factors, like their evolutionary age or the genomic location where they emerged. The role of mutations in the shaping of microRNA-driven regulatory interactions is emphasized with the acknowledgement that, while the whole microRNA sequence is highly conserved, the seed region shows a pattern of higher genetic diversity that appears to be caused by the dramatic frequency shifts of a fraction of human microRNAs. We highlight the participation of these microRNAs in population-specific processes by identifying that not only the seed, but also the loop, are particularly differentiated regions among human populations. The quantitative computational comparison of signatures of population differentiation showed that candidate microRNAs with the largest differences are enriched in variants implicated in gene expression levels (eQTLs), selective sweeps and pathological processes. We explore the implication of these evolutionary-driven microRNAs and their SNPs in human diseases, such as different types of cancer, and discuss their role in population-specific disease risk.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Villegas Miron, P., Gallego, A., Bertranpetit, J., Laayouni, H., Espinosa-Parrilla, Y.. 2021-05-25. Signatures of genetic variation in human microRNAs point to processes of positive selection related to population-specific disease risks. https://doi.org/10.1101/2021.05.24.445417

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Geometry of antigenic evolution improves influenza vaccine selection

Anticipating antigenic evolution is essential for selecting effective seasonal influenza A/H3N2 vaccine strains. To this end, we integrated hemagglutination-inhibition and neutralization titers spanning 2002 to 2025 into a unified Bayesian antigenic map. The map resolves twelve antigenic clusters advancing in discrete steps, with several clusters co-circulating in most seasons. In 15 of 21 seasons, the WHO-recommended vaccine belonged to an earlier cluster than the dominant circulating cluster. The direction of each vaccine update relative to recent viral drift predicted vaccine effectiveness one season ahead in out-of-sample forecasts. Antigenic distance, the conventional measure of vaccine-virus match, was weakly associated with effectiveness until update direction was accounted for. Retrospectively ranking candidate strains by predicted effectiveness would have selected a strain predicted to outperform the WHO recommendation in every season, raising mean predicted effectiveness by 10 percentage points.

evolutionary biology

Evolutionary replay of duplicate-gene retention across independent whole-genome duplications

Whole-genome duplications repeatedly expose ancestral gene lineages to the same broad evolutionary outcome-retention or loss of duplicated copies-but it remains unclear whether this history replays similarly across evolutionary scales. We placed duplicate retention in shared hierarchical orthologous-group coordinates and compared percentile ranks defined within each event-wide mapped universe. Three independent angiosperm whole-genome duplications showed reproducible replay (global rank effect T-replay = 0.210, bootstrap 95% confidence interval 0.172-0.248; permutation P = 1/100,001). A plant reference-panel score specified before target outcomes were examined predicted retention after the Apple/Pear duplication ({rho} = 0.169, n = 373). Deep transfer was heterogeneous: the teleost-genome-duplication estimate was positive but unresolved ({rho} = 0.107, n = 151, 95% confidence interval -0.050 to 0.260), whereas transfer to the ancient budding-yeast whole-genome duplication (yeast WGD) was supported ({rho} = 0.280, n = 186). Independently reconstructed animal outcomes also replayed between teleost and Stylommatophora duplications (r = 0.226, n = 146, P = 0.00326), although the effect remained below a prespecified strong-effect threshold. A strict plant-animal comparison was limited to 25 deeply one-to-one lineages and was unresolved (r = 0.033, 95% confidence interval -0.303 to 0.340). Thus, ancestral gene-lineage identity contributes reproducibly to duplicate retention after independent whole-genome duplications, but replay is structured by evolutionary lineage and modified by event-specific history rather than governed by one universal gene-fate ranking.

evolutionary biology

A Hymenoptera-restricted gene mediating ant castes co-opts deeply conserved machinery to control organ size

Lineage-specific genes are widespread and have been implicated as phenotypic innovation inducers, but how they acquire complex developmental functions remains poorly understood. Ant queens and workers develop dramatically different organ sizes from identical genomes under juvenile hormone (JH) control, yet the molecular effectors translating JH signalling into caste-specific organ growth remain unknown. Here we identify torch, a Hymenoptera-restricted gene, as the most consistently gyne-biased and JH-responsive gene across 68 ant species. Knockdown of torch in virgin queens of Monomorium pharaonis produces a worker-like, multi-organ growth-restricted phenotype. Mechanistically, torch harbours an E-box-like motif activated by the JH receptor Gce-Tai and acts as a GA-repeat-binding transcription factor that regulates Hippo signalling, the deeply conserved organ-size control pathway in animals. Expressing torch heterologously in mice and a growth-restricted Drosophila background shows that the gene retained its general growth-promoting activity across more than 700 million years of animal evolution in lineages that lack the gene, establishing that its function is mediated through conserved rather than ant-specific machinery. A lineage-specific gene can therefore acquire complex morphogenetic function by co-opting ancient organ-size circuitry, providing a general route by which novel genes can drive phenotypic innovation.

evolutionary biology