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allotetraploid Arabidopsis kamchatica 中雄性成分降解导致近期自交不亲和性丧失。

Recent loss of self-incompatibility by degradation of the male component in allotetraploid Arabidopsis kamchatica.

机构信息

Institute of Evolutionary Biology and Environmental Studies, Institute of Plant Biology, and Zurich-Basel Plant Science Center, University of Zurich, Zurich, Switzerland.

出版信息

PLoS Genet. 2012;8(7):e1002838. doi: 10.1371/journal.pgen.1002838. Epub 2012 Jul 26.

DOI:10.1371/journal.pgen.1002838
PMID:22844253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3405996/
Abstract

The evolutionary transition from outcrossing to self-fertilization (selfing) through the loss of self-incompatibility (SI) is one of the most prevalent events in flowering plants, and its genetic basis has been a major focus in evolutionary biology. In the Brassicaceae, the SI system consists of male and female specificity genes at the S-locus and of genes involved in the female downstream signaling pathway. During recent decades, much attention has been paid in particular to clarifying the genes responsible for the loss of SI. Here, we investigated the pattern of polymorphism and functionality of the female specificity gene, the S-locus receptor kinase (SRK), in allotetraploid Arabidopsis kamchatica. While its parental species, A. lyrata and A. halleri, are reported to be diploid and mainly self-incompatible, A. kamchatica is self-compatible. We identified five highly diverged SRK haplogroups, found their disomic inheritance and, for the first time in a wild allotetraploid species, surveyed the geographic distribution of SRK at the two homeologous S-loci across the species range. We found intact full-length SRK sequences in many accessions. Through interspecific crosses with the self-incompatible and diploid congener A. halleri, we found that the female components of the SI system, including SRK and the female downstream signaling pathway, are still functional in these accessions. Given the tight linkage and very rare recombination of the male and female components on the S-locus, this result suggests that the degradation of male components was responsible for the loss of SI in A. kamchatica. Recent extensive studies in multiple Brassicaceae species demonstrate that the loss of SI is often derived from mutations in the male component in wild populations, in contrast to cultivated populations. This is consistent with theoretical predictions that mutations disabling male specificity are expected to be more strongly selected than mutations disabling female specificity, or the female downstream signaling pathway.

摘要

从异交到自交(自花授粉)的进化转变是开花植物中最常见的事件之一,其遗传基础一直是进化生物学的主要焦点。在十字花科植物中,SI 系统由 S 基因座上的雄性和雌性特异性基因以及雌性下游信号通路中的基因组成。在最近几十年中,人们特别关注阐明导致 SI 丧失的基因。在这里,我们研究了四倍体拟南芥 kamchatica 中雌性特异性基因 S 基因座受体激酶(SRK)的多态性和功能模式。虽然其亲本种 A. lyrata 和 A. halleri 被报道为二倍体且主要是自交不亲和的,但 A. kamchatica 是自交亲和的。我们鉴定了五个高度分化的 SRK 单倍型群,发现它们是二倍体遗传的,并且首次在野生异源四倍体物种中,在整个物种范围内调查了两个同源 S 基因座上的 SRK 地理分布。我们在许多标本中发现了完整的全长 SRK 序列。通过与自交不亲和的二倍体同属种 A. halleri 的种间杂交,我们发现 SI 系统的雌性成分,包括 SRK 和雌性下游信号通路,在这些标本中仍然具有功能。鉴于 S 基因座上的雄性和雌性成分紧密连锁且很少重组,这一结果表明,在 A. kamchatica 中,SI 的丧失是由于雄性成分的退化所致。最近在多个十字花科物种中的广泛研究表明,在野生种群中,SI 的丧失通常是由于雄性成分的突变引起的,与栽培种群不同。这与理论预测一致,即失活雄性特异性的突变预计比失活雌性特异性或雌性下游信号通路的突变受到更强的选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/42c95f237b56/pgen.1002838.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/6f9c45b828bf/pgen.1002838.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/58855077a9a9/pgen.1002838.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/25dc1e3b9d88/pgen.1002838.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/647a6d5054d1/pgen.1002838.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/fb565c568326/pgen.1002838.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/42c95f237b56/pgen.1002838.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/6f9c45b828bf/pgen.1002838.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/58855077a9a9/pgen.1002838.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/25dc1e3b9d88/pgen.1002838.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/647a6d5054d1/pgen.1002838.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/fb565c568326/pgen.1002838.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e185/3405996/42c95f237b56/pgen.1002838.g006.jpg

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