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果蝇Yemanuclein与黏连蛋白复合体和联会复合体相关联。

Drosophila Yemanuclein associates with the cohesin and synaptonemal complexes.

作者信息

Meyer Régis E, Algazeery Ahmed, Capri Michèle, Brazier Hélène, Ferry Christine, Aït-Ahmed Ounissa

机构信息

Institut de Génétique Humaine, Unité Propre de Recherche 1142, Centre National de la Recherche Scientifique (CNRS), 34396 Montpellier, France.

Institut de Génétique Humaine, Unité Propre de Recherche 1142, Centre National de la Recherche Scientifique (CNRS), 34396 Montpellier, France Institute of Regenerative Medicine and Biotherapy (IRMB), INSERM U1040/Hôpital Saint-Eloi CHRU, 34295 Montpellier, France

出版信息

J Cell Sci. 2014 Nov 1;127(Pt 21):4658-66. doi: 10.1242/jcs.152520. Epub 2014 Sep 4.

Abstract

Meiosis is characterized by two chromosome segregation rounds (meiosis I and II), which follow a single round of DNA replication, resulting in haploid genome formation. Chromosome reduction occurs at meiosis I. It relies on key structures, such as chiasmata, which are formed by repair of double-strand breaks (DSBs) between the homologous chromatids. In turn, to allow for segregation of homologs, chiasmata rely on the maintenance of sister chromatid cohesion. In most species, chiasma formation requires the prior synapsis of homologous chromosome axes, which is mediated by the synaptonemal complex, a tripartite proteinaceous structure specific to prophase I of meiosis. Yemanuclein (Yem) is a maternal factor that is crucial for sexual reproduction. It is required in the zygote for chromatin assembly of the male pronucleus, where it acts as a histone H3.3 chaperone in complex with Hira. We report here that Yem associates with the synaptonemal complex and the cohesin complex. A genetic interaction between yem(1) (V478E) and the Spo11 homolog mei-W68, modified a yem(1) dominant effect on crossover distribution, suggesting that Yem has an early role in meiotic recombination. This is further supported by the impact of yem mutations on DSB kinetics. A Hira mutation gave a similar effect, presumably through disruption of Hira-Yem complex.

摘要

减数分裂的特征是两轮染色体分离(减数分裂I和II),这两轮分离发生在一轮DNA复制之后,导致单倍体基因组的形成。染色体数目减半发生在减数分裂I。它依赖于关键结构,如交叉,交叉是由同源染色单体之间的双链断裂(DSB)修复形成的。反过来,为了实现同源染色体的分离,交叉依赖于姐妹染色单体黏连的维持。在大多数物种中,交叉的形成需要同源染色体轴先进行联会,这是由联会复合体介导的,联会复合体是减数分裂I前期特有的一种由三部分组成的蛋白质结构。Yemanuclein(Yem)是一种对有性生殖至关重要的母体因子。它在合子中是雄性原核染色质组装所必需的,在那里它作为与Hira形成复合体的组蛋白H3.3伴侣蛋白发挥作用。我们在此报告,Yem与联会复合体和黏连蛋白复合体相关联。yem(1)(V478E)与Spo11同源物mei-W68之间的遗传相互作用,改变了yem(1)对交叉分布的显性效应,这表明Yem在减数分裂重组中起早期作用。yem突变对DSB动力学的影响进一步支持了这一点。Hira突变产生了类似的效果,可能是通过破坏Hira-Yem复合体实现的。

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