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联会缺陷突变体揭示了秀丽隐杆线虫减数分裂过程中染色体构象与双链断裂修复模式之间的相关性。

Synapsis-defective mutants reveal a correlation between chromosome conformation and the mode of double-strand break repair during Caenorhabditis elegans meiosis.

作者信息

Smolikov Sarit, Eizinger Andreas, Hurlburt Allison, Rogers Eric, Villeneuve Anne M, Colaiácovo Mónica P

机构信息

Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Genetics. 2007 Aug;176(4):2027-33. doi: 10.1534/genetics.107.076968. Epub 2007 Jun 11.

Abstract

SYP-3 is a new structural component of the synaptonemal complex (SC) required for the regulation of chromosome synapsis. Both chromosome morphogenesis and nuclear organization are altered throughout the germlines of syp-3 mutants. Here, our analysis of syp-3 mutants provides insights into the relationship between chromosome conformation and the repair of meiotic double-strand breaks (DSBs). Although crossover recombination is severely reduced in syp-3 mutants, the production of viable offspring accompanied by the disappearance of RAD-51 foci suggests that DSBs are being repaired in these synapsis-defective mutants. Our studies indicate that once interhomolog recombination is impaired, both intersister recombination and nonhomologous end-joining pathways may contribute to repair during germline meiosis. Moreover, our studies suggest that the conformation of chromosomes may influence the mode of DSB repair employed during meiosis.

摘要

SYP-3是联会复合体(SC)的一种新结构成分,是调节染色体联会所必需的。在syp-3突变体的整个生殖系中,染色体形态发生和核组织都会发生改变。在这里,我们对syp-3突变体的分析为染色体构象与减数分裂双链断裂(DSB)修复之间的关系提供了见解。虽然在syp-3突变体中交叉重组严重减少,但伴随着RAD-51焦点消失的活后代的产生表明这些联会缺陷突变体中的DSB正在被修复。我们的研究表明,一旦同源重组受损,姐妹染色单体间重组和非同源末端连接途径都可能在生殖系减数分裂期间参与修复。此外,我们的研究表明染色体的构象可能会影响减数分裂期间使用的DSB修复模式。

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