Roles of Hop1 and Mek1 in Meiotic Chromosome Pairing and Recombination Partner Choice in Schizosaccharomyces pombe
Roles of Hop1 and Mek1 in Meiotic Chromosome Pairing and Recombination Partner Choice in Schizosaccharomyces pombe
复制标题
DOI：
10.1128/mcb.00919-09
复制
发表时间：
2010-04-01
影响因子：
5.3
通讯作者：
Kohli, Juerg
中科院分区：
文献类型：
--
作者：
Latypov, Vitaly;Rothenberg, Maja;Kohli, Juerg
合丝复合体（SC）蛋白Hop1和Mek1被认为通过建立一个阻止姐妹染色单体重组的屏障来促进酿酒酵母减数分裂中的同源重组。因此，了解这些同源蛋白在粟酒裂殖酵母中是否发挥类似的作用是很有意义的。在染色体内重组（ICR）检测中，发现hop1和mek1单缺失和双缺失突变体的不相等姐妹染色单体重组（USCR）增加。同源染色体之间的减数分裂基因间（交换）和基因内（转换）重组减少。双链断裂（DSB）水平也降低。值得注意的是，hop1的缺失恢复了rad50S减数分裂中的DSB修复。这可能表明hop1和mek1缺失菌株的DSB修复动力学改变。提出了一种假说，提出由Hop1和Mek1瞬时抑制DSB处理，从而通过与同源染色体的相互作用提供更多的时间进行修复。Hop1和Mek1的缺失将导致更快的修复和与姐妹染色单体的更多相互作用。因此，在S.粟酒裂殖酵母减数分裂中，姐妹Holliday连接超过同源Holliday连接的形成已被证明，Hop1和Mek1可能增强同源相互作用，以确保野生型水平的交叉形成，而不是抑制姐妹染色单体相互作用。
Synaptonemal complex (SC) proteins Hop1 and Mek1 have been proposed to promote homologous recombination in meiosis of Saccharomyces cerevisiae by establishment of a barrier against sister chromatid recombination. Therefore, it is interesting to know whether the homologous proteins play a similar role in Schizosaccharomyces pombe. Unequal sister chromatid recombination (USCR) was found to be increased in hop1 and mek1 single and double deletion mutants in assays for intrachromosomal recombination (ICR). Meiotic intergenic (crossover) and intragenic (conversion) recombination between homologous chromosomes was reduced. Double-strand break (DSB) levels were also lowered. Notably, deletion of hop1 restored DSB repair in rad50S meiosis. This may indicate altered DSB repair kinetics in hop1 and mek1 deletion strains. A hypothesis is advanced proposing transient inhibition of DSB processing by Hop1 and Mek1 and thus providing more time for repair by interaction with the homologous chromosome. Loss of Hop1 and Mek1 would then result in faster repair and more interaction with the sister chromatid. Thus, in S. pombe meiosis, where an excess of sister Holliday junction over homologous Holliday junction formation has been demonstrated, Hop1 and Mek1 possibly enhance homolog interactions to ensure wild-type level of crossover formation rather than inhibiting sister chromatid interactions.