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联合分子解析需要 MUS-81 和 XPF-1 在秀丽隐杆线虫减数分裂过程中的冗余活性。

Joint molecule resolution requires the redundant activities of MUS-81 and XPF-1 during Caenorhabditis elegans meiosis.

机构信息

Department of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.

出版信息

PLoS Genet. 2013;9(7):e1003582. doi: 10.1371/journal.pgen.1003582. Epub 2013 Jul 18.

Abstract

The generation and resolution of joint molecule recombination intermediates is required to ensure bipolar chromosome segregation during meiosis. During wild type meiosis in Caenorhabditis elegans, SPO-11-generated double stranded breaks are resolved to generate a single crossover per bivalent and the remaining recombination intermediates are resolved as noncrossovers. We discovered that early recombination intermediates are limited by the C. elegans BLM ortholog, HIM-6, and in the absence of HIM-6 by the structure specific endonuclease MUS-81. In the absence of both MUS-81 and HIM-6, recombination intermediates persist, leading to chromosome breakage at diakinesis and inviable embryos. MUS-81 has an additional role in resolving late recombination intermediates in C. elegans. mus-81 mutants exhibited reduced crossover recombination frequencies suggesting that MUS-81 is required to generate a subset of meiotic crossovers. Similarly, the Mus81-related endonuclease XPF-1 is also required for a subset of meiotic crossovers. Although C. elegans gen-1 mutants have no detectable meiotic defect either alone or in combination with him-6, mus-81 or xpf-1 mutations, mus-81;xpf-1 double mutants are synthetic lethal. While mus-81;xpf-1 double mutants are proficient for the processing of early recombination intermediates, they exhibit defects in the post-pachytene chromosome reorganization and the asymmetric disassembly of the synaptonemal complex, presumably triggered by crossovers or crossover precursors. Consistent with a defect in resolving late recombination intermediates, mus-81; xpf-1 diakinetic bivalents are aberrant with fine DNA bridges visible between two distinct DAPI staining bodies. We were able to suppress the aberrant bivalent phenotype by microinjection of activated human GEN1 protein, which can cleave Holliday junctions, suggesting that the DNA bridges in mus-81; xpf-1 diakinetic oocytes are unresolved Holliday junctions. We propose that the MUS-81 and XPF-1 endonucleases act redundantly to process late recombination intermediates to form crossovers during C. elegans meiosis.

摘要

为确保减数分裂过程中染色体的两极分离,需要形成并解决联会分子重组中间体。在秀丽隐杆线虫的野生型减数分裂过程中,由 SPO-11 产生的双链断裂被解决,从而在每个二价体中产生一个单交叉,其余的重组中间体则被解决为非交叉。我们发现,早期重组中间体受到秀丽隐杆线虫 BLM 同源物 HIM-6 的限制,在 HIM-6 缺失的情况下受到结构特异性内切酶 MUS-81 的限制。在 MUS-81 和 HIM-6 都缺失的情况下,重组中间体持续存在,导致在减数分裂前期二价体断裂和胚胎不育。MUS-81 在解决秀丽隐杆线虫晚期重组中间体方面具有额外的作用。mus-81 突变体表现出降低的交叉重组频率,表明 MUS-81 是产生部分减数分裂交叉所必需的。同样,MUS81 相关内切酶 XPF-1 也需要部分减数分裂交叉。尽管 C. elegans gen-1 突变体单独或与 him-6、mus-81 或 xpf-1 突变体组合时没有检测到减数分裂缺陷,但 mus-81;xpf-1 双突变体是合成致死的。虽然 mus-81;xpf-1 双突变体能够有效地处理早期重组中间体,但它们在后减数前期染色体重排和联会复合体的不对称解体方面存在缺陷,这可能是由交叉或交叉前体触发的。与解决晚期重组中间体缺陷一致,mus-81;xpf-1 减数前期二价体异常,在两个不同的 DAPI 染色体之间可见细 DNA 桥。我们能够通过注射激活的人 GEN1 蛋白来抑制异常的二价体表型,该蛋白可以切割 Holliday 连接,这表明 mus-81;xpf-1 减数前期卵母细胞中的 DNA 桥是未解决的 Holliday 连接。我们提出,MUS-81 和 XPF-1 内切酶冗余地作用于晚期重组中间体,以在 C. elegans 减数分裂过程中形成交叉。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af2e/3715453/508fdea875e8/pgen.1003582.g001.jpg

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