果蝇 MCM 复合物的进化通过阻止 BLM 解旋酶来促进减数分裂交叉。
Evolution of an MCM complex in flies that promotes meiotic crossovers by blocking BLM helicase.
机构信息
Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599, USA.
出版信息
Science. 2012 Dec 7;338(6112):1363-5. doi: 10.1126/science.1228190.
Abstract
Generation of meiotic crossovers in many eukaryotes requires the elimination of anti-crossover activities by using the Msh4-Msh5 heterodimer to block helicases. Msh4 and Msh5 have been lost from the flies Drosophila and Glossina, but we identified a complex of minichromosome maintenance (MCM) proteins that functionally replace Msh4-Msh5. We found that REC, an ortholog of MCM8 that evolved under strong positive selection in flies, interacts with MEI-217 and MEI-218, which arose from a previously undescribed metazoan-specific MCM protein. Meiotic crossovers were reduced in Drosophila rec, mei-217, and mei-218 mutants; however, removal of the Bloom syndrome helicase (BLM) ortholog restored crossovers. Thus, MCMs were co-opted into a novel complex that replaced the meiotic pro-crossover function of Msh4-Msh5 in flies.
摘要
在许多真核生物中，减数分裂交叉的产生需要利用 Msh4-Msh5 异二聚体来消除抗交叉活性，以阻止解旋酶的作用。果蝇和舌蝇已经失去了 Msh4 和 Msh5，但我们鉴定出一个由微小染色体维持 (MCM) 蛋白组成的复合物，该复合物在功能上替代了 Msh4-Msh5。我们发现，在果蝇中经历强烈正选择进化的 REC，是 MCM8 的同源物，与 MEI-217 和 MEI-218 相互作用，而 MEI-217 和 MEI-218 则来自于以前未描述的后生动物特异性 MCM 蛋白。果蝇 rec、mei-217 和 mei-218 突变体中的减数分裂交叉减少；然而，去除 Bloom 综合征解旋酶 (BLM) 同源物恢复了交叉。因此，MCM 被招募到一个新的复合物中，该复合物取代了 Msh4-Msh5 在果蝇中的减数分裂前交叉功能。
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