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染色质域蛋白 MRG-1 促进秀丽隐杆线虫减数分裂中 SC 独立的同源配对。

The chromodomain protein MRG-1 facilitates SC-independent homologous pairing during meiosis in Caenorhabditis elegans.

机构信息

Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.

出版信息

Dev Cell. 2011 Dec 13;21(6):1092-103. doi: 10.1016/j.devcel.2011.09.019.

Abstract

Homologous chromosome pairing is a prerequisite to establish physical linkage between homologs, which is critical for faithful chromosome segregation during meiosis I. The establishment of pairing is genetically separable from subsequent synapsis, defined as stabilization of pairing by the synaptonemal complex (SC). The underlying mechanism of presynaptic pairing is poorly understood. In the nematode Caenorhabditis elegans, a unique cis-acting element, the pairing center (PC), is essential for presynaptic pairing; however, it is not known whether and how the remainder of the chromosome contributes to presynaptic pairing. Here we report direct evidence for presynaptic pairing activity intrinsic to non-PC regions, which is facilitated by a conserved chromodomain protein, MRG-1. In mrg-1 loss-of-function mutants, pairing is compromised specifically in non-PC regions, leading to nonhomologous SC assembly. Our data support a model in which presynaptic alignment in non-PC regions collaborates with initial PC pairing to ensure correct homologous synapsis.

摘要

同源染色体配对是建立同源染色体之间物理连接的前提条件,这对于减数分裂 I 期间同源染色体的正确分离至关重要。配对的建立在遗传上与随后的联会分离,联会被联会复合体 (SC) 定义为配对的稳定化。配对的前突触机制知之甚少。在线虫秀丽隐杆线虫中,一个独特的顺式作用元件,配对中心 (PC),是前突触配对所必需的;然而,目前尚不清楚其余染色体是否以及如何参与前突触配对。在这里,我们报告了非 PC 区域固有前突触配对活性的直接证据,这是由保守的 chromodomain 蛋白 MRG-1 促进的。在 mrg-1 功能丧失突变体中,配对在非 PC 区域受到损害,导致非同源 SC 组装。我们的数据支持这样一种模型,即非 PC 区域的前突触排列与初始 PC 配对合作,以确保同源联会的正确。

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