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小泛素样修饰蛋白在减数分裂染色体联会中的作用。

A Role for SUMO in meiotic chromosome synapsis.

作者信息

Hooker Gillian W, Roeder G Shirleen

机构信息

Department of Molecular, Cellular, and Developmental Biology, Yale University, 266 Whitney Avenue, New Haven, Connecticut 06511, USA.

出版信息

Curr Biol. 2006 Jun 20;16(12):1238-43. doi: 10.1016/j.cub.2006.04.045.

Abstract

During meiotic prophase, homologous chromosomes engage in a complex series of interactions that ensure their proper segregation at meiosis I. A central player in these interactions is the synaptonemal complex (SC), a proteinaceous structure elaborated along the lengths of paired homologs. In mutants that fail to make SC, crossing over is decreased, and chromosomes frequently fail to recombine; consequently, many meiotic products are inviable because of aneuploidy. Here, we have investigated the role of the small ubiquitin-like protein modifier (SUMO) in SC formation during meiosis in budding yeast. We show that SUMO localizes specifically to synapsed regions of meiotic chromosomes and that this localization depends on Zip1, a major building block of the SC. A non-null allele of the UBC9 gene, which encodes the SUMO-conjugating enzyme, impairs Zip1 polymerization along chromosomes. The Ubc9 protein localizes to meiotic chromosomes, coincident with SUMO staining. In the zip1 mutant, SUMO localizes to discrete foci on chromosomes. These foci coincide with axial associations, where proteins involved in synapsis initiation are located. Our data suggest a model in which SUMO modification of chromosomal proteins promotes polymerization of Zip1 along chromosomes. The ubc9 mutant phenotype provides the first evidence for a cause-and-effect relationship between sumoylation and synapsis.

摘要

在减数分裂前期,同源染色体参与一系列复杂的相互作用,以确保它们在减数分裂I时正确分离。这些相互作用中的核心参与者是联会复合体(SC),一种沿着配对同源染色体的长度形成的蛋白质结构。在无法形成SC的突变体中,交叉互换减少,染色体经常无法重组;因此,许多减数分裂产物由于非整倍体而无法存活。在这里,我们研究了小泛素样修饰蛋白(SUMO)在芽殖酵母减数分裂过程中SC形成中的作用。我们发现SUMO特异性定位于减数分裂染色体的联会区域,并且这种定位依赖于Zip1,SC的主要组成部分。编码SUMO结合酶的UBC9基因的一个非无效等位基因会损害Zip1沿染色体的聚合。Ubc9蛋白定位于减数分裂染色体,与SUMO染色一致。在zip1突变体中,SUMO定位于染色体上的离散焦点。这些焦点与轴向关联重合,参与联会起始的蛋白质位于此处。我们的数据提出了一个模型,其中染色体蛋白的SUMO修饰促进Zip1沿染色体的聚合。ubc9突变体表型为SUMO化与联会之间的因果关系提供了首个证据。

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