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基因组范围内对果蝇杂种不育的剖析证实了一个多基因阈值结构。

Genome-wide dissection of hybrid sterility in Drosophila confirms a polygenic threshold architecture.

机构信息

the Grup de Biologia Evolutiva, Departament de Genètica i de Microbiologia, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.

出版信息

J Hered. 2014 May-Jun;105(3):381-96. doi: 10.1093/jhered/esu003. Epub 2014 Jan 31.

Abstract

To date, different studies about the genetic basis of hybrid male sterility (HMS), a postzygotic reproductive barrier thoroughly investigated using Drosophila species, have demonstrated that no single major gene can produce hybrid sterility without the cooperation of several genetic factors. Early work using hybrids between Drosophila koepferae (Dk) and Drosophila buzzatii (Db) was consistent with the idea that HMS requires the cooperation of several genetic factors, supporting a polygenic threshold (PT) model. Here we present a genome-wide mapping strategy to test the PT model, analyzing serially backcrossed fertile and sterile males in which the Dk genome was introgressed into the Db background. We identified 32 Dk-specific markers significantly associated with hybrid sterility. Our results demonstrate 1) a strong correlation between the number of segregated sterility markers and males' degree of sterility, 2) the exchangeability among markers, 3) their tendency to cluster into low-recombining chromosomal regions, and 4) the requirement for a minimum number (threshold) of markers to elicit sterility. Although our findings do not contradict a role for occasional major hybrid-sterility genes, they conform more to the view that HMS primarily evolves by the cumulative action of many interacting genes of minor effect in a complex PT architecture.

摘要

迄今为止,已有不同的研究探讨了杂种雄性不育(HMS)的遗传基础,该障碍是在使用果蝇属物种进行深入研究的合子后生殖障碍。这些研究表明,没有单一的主要基因可以在没有几个遗传因素合作的情况下产生杂种不育。早期使用 Drosophila koepferae(Dk)和 Drosophila buzzatii(Db)杂种的研究工作与 HMS 需要几个遗传因素合作的观点一致,支持多基因阈值(PT)模型。在这里,我们提出了一种全基因组作图策略来检验 PT 模型,分析连续回交的可育和不育雄性,其中 Dk 基因组被导入 Db 背景。我们鉴定了 32 个与杂种不育显著相关的 Dk 特异性标记。我们的结果表明:1)分离不育标记的数量与雄性不育程度之间存在很强的相关性;2)标记之间可交换;3)它们倾向于聚类到低重组染色体区域;4)需要达到一个最小数量(阈值)的标记才能引发不育。尽管我们的发现并不否认偶然的主要杂种不育基因的作用,但它们更符合 HMS 主要通过许多相互作用的微小效应基因在复杂的 PT 结构中的累积作用进化的观点。

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