DrRad51 Is Required for Chiasmata Formation in Meiosis in Planarian Dugesia ryukyuensis
DrRad51 Is Required for Chiasmata Formation in Meiosis in Planarian Dugesia ryukyuensis
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DOI：
10.1002/mrd.22308
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发表时间：
2014-05-01
影响因子：
2.5
通讯作者：
Matsumoto, Midori
中科院分区：
文献类型：
--
作者：
Chinone, Ayako;Matsumoto, Midori
Rad 51是一种保守的真核蛋白，介导有丝分裂和减数分裂过程中DNA双链断裂的同源重组修复。在减数分裂前期I，同源重组增强了同源染色体之间的连锁，以提高后期I分离的准确性。然而，在多倍体情况下，同源染色体分离的困难往往会破坏减数分裂。然而，三倍体个体的三角涡虫琉球三角涡虫能够产生功能配子通过一个特殊的形式减数分裂。为阐明三倍体D.研究了rad 51基因的功能。我们分离了Rad 51家族的三个基因，Rad 51同源物Dr-rad 51和Rad 51旁系同源物Dr-rad 51 B和Dr-rad 51 C。dr-rad 51在生殖系和体干细胞中表达，但不是体组织再生所必需的。RNA干扰（RNAi）的Dr-rad 51在性化过程中的耗竭并不影响染色体的行为在偶线期卵母细胞，但确实导致在双线期的交叉损失。因此，同源重组似乎不是突触形成所必需的，但在D.琉球。摩尔Reprod. Dev.第81章：？2014. (c)2014年威利期刊公司
Rad51, a conserved eukaryotic protein, mediates the homologous-recombination repair of DNA double-strand breaks that occur during both mitosis and meiosis. During prophase I of meiosis, homologous recombination enhances the linkage between homologous chromosomes to increase the accuracy of segregation at anaphase I. In polyploidy situations, however, difficulties with homologous chromosome segregation often disrupt meiosis. Yet, triploid individuals of the planarian Dugesia ryukyuensis are able to produce functional gametes through a specialized form of meiosis. To shed light on the molecular mechanisms that promote successful meiosis in triploid D. ryukyuensis, we investigated rad51 gene function. We isolated three genes of the Rad51 family, the Rad51 homolog Dr-rad51 and the Rad51 paralogs Dr-rad51B and Dr-rad51C. Dr-rad51 was expressed in germ-line and presumably in somatic stem cells, but was not necessary for the regeneration of somatic tissue. RNA-interference (RNAi) depletion of Dr-rad51 during sexualization did not affect chromosome behavior in zygotene oocytes, but did result in the loss of chiasmata at the diplotene stage. Thus, homologous recombination does not appear to be necessary for synapsis, but is needed for crossover and proper segregation in D. ryukyuensis. Mol. Reprod. Dev. 81: ???-???, 2014. (c) 2014 Wiley Periodicals, Inc.