Experimental evolution unveils a role for structural variants and sex-specificity in the genetic architecture of lifespan
- 1University of Uppsala
Abstract
Insights into the genetic basis of lifespan evolution can link evolutionary theory with an understanding of health, disease and adaptation. We leverage the power of >200 generations of experimental evolution in a seed beetle to unveil the genomic architecture of lifespan evolution. Replicated populations evolved under regimes favoring either a short or long life, resulting in a near doubling of lifespan. Whole genome re-sequencing revealed that short- and long-lived lines were strongly differentiated (global FST = 0.41) and more than 700 genes showed consistent signs of divergent selection. Remarkably, short- and long-lived lines were consistently divergent in a large number of regions harboring copy-number variants (CNVs), involving >600 genes. The evolution of a long life involved many distinct biological processes, such as DNA fidelity, mitotic integrity, reproduction, metabolism, immunity and stress response. A pedigree-based genome scan for quantitative trait loci (QTLs) uncovered several QTLs with large effects on lifespan, but the genetic basis of a long life was dominated by a very large number of regions with medium and small effects. The genome-wide spatial association with QTL effects was, if anything, stronger for CNVs than for sequence variants. The genetic effects of QTLs on lifespan were positively correlated overall between the sexes, but four regions showed pronounced sex-differences. Our results show that structural variants play a significant role in the evolution of an extended lifespan and the highly polygenic genomic architecture is to some extent sex-specific, consistent with differences in physiology and life history tradeoffs between the sexes.
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BibTeX
@misc{toros2026experimental,
title = {{Experimental evolution unveils a role for structural variants and sex-specificity in the genetic architecture of lifespan}},
author = {A. Toros and M. E. Pettersson and A. P. Fuentes-Pardo and A. Rego and C.-J. Rubin and A. Sayadi and M. Dordevic and U. Savkovic and B. Stojkovic and E. Immonen and M. Kucka and Y. F. Chan and L. Andersson and G. Arnqvist},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.28.762418},
url = {https://www.biorxiv.org/content/10.64898/2026.10.28.762418v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Experimental evolution unveils a role for structural variants and sex-specificity in the genetic architecture of lifespan
AU - A. Toros
AU - M. E. Pettersson
AU - A. P. Fuentes-Pardo
AU - A. Rego
AU - C.-J. Rubin
AU - A. Sayadi
AU - M. Dordevic
AU - U. Savkovic
AU - B. Stojkovic
AU - E. Immonen
AU - M. Kucka
AU - Y. F. Chan
AU - L. Andersson
AU - G. Arnqvist
PY - 2026
DA - 2026/10/28
PB - bioRxiv
DO - 10.64898/2026.10.28.762418
UR - https://www.biorxiv.org/content/10.64898/2026.10.28.762418v1
AB - Insights into the genetic basis of lifespan evolution can link evolutionary theory with an understanding of health, disease and adaptation. We leverage the power of >200 generations of experimental evolution in a seed beetle to unveil the genomic architecture of lifespan evolution. Replicated populations evolved under regimes favoring either a short or long life, resulting in a near doubling of lifespan. Whole genome re-sequencing revealed that short- and long-lived lines were strongly differentiated (global FST = 0.41) and more than 700 genes showed consistent signs of divergent selection. Remarkably, short- and long-lived lines were consistently divergent in a large number of regions harboring copy-number variants (CNVs), involving >600 genes. The evolution of a long life involved many distinct biological processes, such as DNA fidelity, mitotic integrity, reproduction, metabolism, immunity and stress response. A pedigree-based genome scan for quantitative trait loci (QTLs) uncovered several QTLs with large effects on lifespan, but the genetic basis of a long life was dominated by a very large number of regions with medium and small effects. The genome-wide spatial association with QTL effects was, if anything, stronger for CNVs than for sequence variants. The genetic effects of QTLs on lifespan were positively correlated overall between the sexes, but four regions showed pronounced sex-differences. Our results show that structural variants play a significant role in the evolution of an extended lifespan and the highly polygenic genomic architecture is to some extent sex-specific, consistent with differences in physiology and life history tradeoffs between the sexes.
ER -