Mus81/Mms4 endonuclease and Sgs1 helicase collaborate to ensure proper recombination intermediate metabolism during meiosis.
Mus81/Mms4 endonuclease and Sgs1 helicase collaborate to ensure proper recombination intermediate metabolism during meiosis.
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DOI：
10.1016/j.molcel.2008.05.021
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发表时间：
2008-08-08
期刊：
影响因子：
16
通讯作者：
Lichten, Michael
中科院分区：
文献类型：
--
作者：
Jessop, Lea;Lichten, Michael
缺乏Sgs 1解旋酶和Mus 81/Mms 4内切酶的芽殖酵母是不能存活的，间接研究表明同源重组出错是死亡的原因。我们发现，缺乏这两种酶的突变体有深刻的缺陷，减数分裂重组中间代谢和交叉（CO）的形成。关节中间体（关节分子; JM）在这些细胞中积累，许多具有野生型细胞中罕见的结构。这些JMs持续存在，防止核分裂。使用诱导型表达系统，我们恢复Mus 81或Sgs 1到sgs 1 mus 81细胞在JM形成的时候。Mus 81的表达并没有阻止JM的形成，但恢复JM分辨率，CO的形成，和核分裂。相反，Sgs 1表达减少JM积累的程度。这些结果表明，Sgs 1和Mus 81/Mms 4合作指导减数分裂重组对同源物间的相互作用，促进适当的染色体分离，也表明，Mus 81/Mms 4促进JM决议在体内。
Budding yeast lacking the Sgs1 helicase and the Mus81/Mms4 endonuclease are inviable, and indirect studies implicate homologous recombination gone awry as the cause of death. We show that mutants lacking both enzymes have profound defects in meiotic recombination intermediate metabolism and crossover (CO) formation. Recombination intermediates (joint molecules; JMs) accumulate in these cells, many with structures that are infrequent in wild type cells. These JMs persist, preventing nuclear division. Using an inducible expression system, we restored Mus81 or Sgs1 to sgs1 mus81 cells at a time when JMs are forming. Mus81 expression did not prevent JM formation, but restored JM resolution, CO formation, and nuclear division. In contrast, Sgs1 expression reduced the extent of JM accumulation. These results indicate that Sgs1 and Mus81/Mms4 collaborate to direct meiotic recombination towards interhomolog interactions that promote proper chromosome segregation, and also indicate that Mus81/Mms4 promotes JM resolution in vivo.
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