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Evolution of self-compatibility in Arabidopsis by a mutation in the male specificity gene

机译:雄性特异性基因突变引起拟南芥自交亲和性的进化

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摘要

Ever since Darwin's pioneering research, the evolution of self-fertilisation (selfing) has been regarded as one of the most prevalent evolutionary transitions in flowering plants. A major mechanism to prevent selfing is the self-incompatibility (SI) recognition system, which consists of male and female specificity genes at the S-locus and SI modifier genes. Under conditions that favour selfing, mutations disabling the male recognition component are predicted to enjoy a relative advantage over those disabling the female component, because male mutations would increase through both pollen and seeds whereas female mutations would increase only through seeds. Despite many studies on the genetic basis of loss of SI in the predominantly selfing plant Arabidopsis thaliana, it remains unknown whether selfing arose through mutations in the female specificity gene (S-receptor kinase, SRK), male specificity gene (S-locus cysteine-rich protein, SCR; also known as S-locus protein 11, SP11) or modifier genes, and whether any of them rose to high frequency across large geographic regions. Here we report that a disruptive 213-base-pair (bp) inversion in the SCR gene (or its derivative haplotypes with deletions encompassing the entire SCR-A and a large portion of SRK-A) is found in 95% of European accessions, which contrasts with the genome-wide pattern of polymorphism in European A. thaliana. Importantly, interspecific crossings using Arabidopsis halleri as a pollen donor reveal that some A. thaliana accessions, including Wei-1, retain the female SI reaction, suggesting that all female components including SRK are still functional. Moreover, when the 213-bp inversion in SCR was inverted and expressed in transgenic Wei-1 plants, the functional SCR restored the SI reaction. The inversion within SCR is the first mutation disrupting SI shown to be nearly fixed in geographically wide samples, and its prevalence is consistent with theoretical predictions regarding the evolutionary advantage of mutations in male components.
机译:自达尔文(Darwin)的开创性研究以来,自肥(selfing)的进化一直被视为开花植物中最普遍的进化转变之一。防止自交的主要机制是自我不相容(SI)识别系统,该系统由S位点的男性和女性特异性基因以及SI修饰子基因组成。在有利于自交的条件下,禁用雄性识别成分的突变预计比禁用雌性成分的突变具有相对优势,因为雄性突变会通过花粉和种子增加,而雌性突变只会通过种子增加。尽管有许多关于主要自交植物拟南芥中SI缺失的遗传基础的研究,但仍不清楚是否通过女性特异性基因(S-受体激酶,SRK),男性特异性基因(S-基因半胱氨酸-蛋白质(SCR);也称为S-基因座蛋白质11(SP11)或修饰基因,以及它们中的任何一个是否在较大的地理区域内上升到很高的频率。在此我们报道,在95%的欧洲国家/地区发现SCR基因(或其衍生的单倍型,其缺失包含整个SCR-A和大部分SRK-A)具有破坏性的213个碱基对(bp)的倒置,与欧洲拟南芥中的全基因组多态性模式形成对比。重要的是,使用拟南芥作为花粉供体的种间杂交显示,一些拟南芥种质,包括Wei-1,保留了雌性SI反应,表明包括SRK在内的所有雌性成分仍在起作用。此外,当SCR中的213bp反向转化并在转基因Wei-1植物中表达时,功能性SCR恢复了SI反应。 SCR中的倒位是第一个突变干扰SI,在地理范围广泛的样本中显示几乎是固定的,其流行程度与有关男性组分突变的进化优势的理论预测相符。

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  • 来源
    《Nature》 |2010年第7293期|p.1342-1346|共5页
  • 作者单位

    Institute of Plant Biology, University Research Priority Program in Systems Biology/Functional Genomics & Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland Department of General Systems Studies, University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan;

    Graduate School of Life Sciences, Tohoku University, Katahira, Sendai 980-8577, Japan Graduate School of Bioresources, Mie University, Tsu 514-8507, Japan;

    Institute of Plant Biology, University Research Priority Program in Systems Biology/Functional Genomics & Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland;

    Graduate School of Life Sciences, Tohoku University, Katahira, Sendai 980-8577, Japan Faculty of Science, Tohoku University, Aoba, Sendai 980-8578, Japan;

    Section of Evolutionary Biology, BioCenter, University of Munich (LMU), Grosshaderner Strasse 2, D-82152 Planegg-Martinsried, Germany;

    Plant Ecological Genetics, Institute of Integrative Biology, ETH Zurich, Universitaetstrasse 16, CH-8092 Zurich, Switzerland;

    Division of Natural Science, Osaka Kyoiku University, Kashiwara 582-8582, Japan;

    Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma 630-0101, Japan;

    Graduate School of Life Sciences, Tohoku University, Katahira, Sendai 980-8577, Japan Faculty of Science, Tohoku University, Aoba, Sendai 980-8578, Japan;

    Institute of Plant Biology, University Research Priority Program in Systems Biology/Functional Genomics & Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland;

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