期刊
MOLECULAR BIOLOGY AND EVOLUTION
卷 29, 期 7, 页码 1781-1789出版社
OXFORD UNIV PRESS
DOI: 10.1093/molbev/mss019
关键词
loss-of-function; neutral variation; genetic drift; life history; yeast; nonadditive heredity; heterosis
资金
- Centre national de la recherche scientifique (CNRS)
- Programme Atip-Avenir
- Association pour la Recherche sur le Cancer (ARC)
- Royal Swedish Academy of Sciences
- Carl Trygger Foundation
- Biotechnology and Biological Sciences Research Council [BB/F015216/1] Funding Source: researchfish
- BBSRC [BB/F015216/1] Funding Source: UKRI
A fundamental question in biology is whether variation in organisms primarily emerges as a function of adaptation or as a function of neutral genetic drift. Trait variation in the model organism baker's yeast follows population bottlenecks rather than environmental boundaries suggesting that it primarily results from genetic drift. Based on the yeast life history, we hypothesized that population-specific loss-of-function mutations emerging in genes recently released from selection is the predominant cause of trait variation within the species. As retention of one functional copy of a gene in diploid yeasts is typically sufficient to maintain completely unperturbed performance, we also conjectured that a crossing of natural yeasts from populations with different loss-of-function mutations would provide a further efficient test bed for this hypothesis. Charting the first species-wide map of trait inheritance in a eukaryotic organism, we found trait heredity to be strongly biased toward diploid hybrid performance exactly mimicking the performance of the best of the parents, as expected given a complete dominance of functional over nonfunctional alleles. Best parent heterosis, partial dominance, and negative nonadditivity were all rare phenomena. Nonadditive inheritance was observed primarily in crosses involving at least one very poor performing parent, most frequently of the West African population, and when molecularly dissected, loss-of-function alleles were identified as the underlying cause. These findings provide support for that population-specific loss-of-function mutations do have a strong impact on genotype-phenotype maps and underscores the role of neutral genetic drift as a driver for trait variation within species.
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