| Literature DB >> 27182945 |
Matthieu Simon1, Stéphanie Durand1, Natacha Pluta1, Nicolas Gobron2, Lucy Botran1, Anthony Ricou1, Christine Camilleri1, Françoise Budar3.
Abstract
Species differentiation and the underlying genetics of reproductive isolation are central topics in evolutionary biology. Hybrid sterility is one kind of reproductive barrier that can lead to differentiation between species. Here, we analyze the complex genetic basis of the intraspecific hybrid male sterility that occurs in the offspring of two distant natural strains of Arabidopsis thaliana, Shahdara and Mr-0, with Shahdara as the female parent. Using both classical and quantitative genetic approaches as well as cytological observation of pollen viability, we demonstrate that this particular hybrid sterility results from two causes of pollen mortality. First, the Shahdara cytoplasm induces gametophytic cytoplasmic male sterility (CMS) controlled by several nuclear loci. Second, several segregation distorters leading to allele-specific pollen abortion (pollen killers) operate in hybrids with either cytoplasm. The complete sterility of the hybrid with the Shahdara cytoplasm results from the genetic linkage of the two causes of pollen mortality, i.e., CMS nuclear determinants and pollen killers. Furthermore, natural variation at these loci in A. thaliana is associated with different male-sterility phenotypes in intraspecific hybrids. Our results suggest that the genomic conflicts that underlie segregation distorters and CMS can concurrently lead to reproductive barriers between distant strains within a species. This study provides a new framework for identifying molecular mechanisms and the evolutionary history of loci that contribute to reproductive isolation, and possibly to speciation. It also suggests that two types of genomic conflicts, CMS and segregation distorters, may coevolve in natural populations.Entities:
Keywords: cytoplasmic male sterility; hybrid sterility; pollen killer; reproductive barrier; segregation distorsion
Mesh:
Year: 2016 PMID: 27182945 PMCID: PMC4937478 DOI: 10.1534/genetics.115.183707
Source DB: PubMed Journal: Genetics ISSN: 0016-6731 Impact factor: 4.562