遗传发育所在PLOS子刊发现水稻同源重组保障的蛋白OsHUS1
减数分裂过程中,同源染色体重组是一复杂而又关键的生物学过程,由于基因组中存在着很多不同类型的重复序列,如何保障重组仅发生在等位的同源序列之间,而避免发生在非等位的同源序列之间,对于这种同源重组的保真机制目前还缺少直接证据与合理解释。
程祝宽课题组利用图位克隆方法,在水稻中鉴定了9-1-1复合体重要成员Hus1的同源蛋白OsHUS1。9-1-1复合体在哺乳动物中广泛参与了DNA的损伤修复,由于相关突变体均会导致胚胎致死,很难研究这些蛋白参与减数分裂的生物学功能。
有趣的是,水稻Oshus1突变体营养生长正常,并且在减数分裂粗线期同源染色体配对及联会复合体形成基本正常,但在终变期至中期I非同源染色体间相互粘连,形成多价体;后期I多价体分开,形成大量染色体桥及染色体碎片,最终导致不育配子的产生。双突变体分析表明这种多价体形成是依赖于DSB的,而不依赖于同源重组所必须的ZMM家族成员。并且在Oshus1突变体中,参与同源染色体配对、联会复合体组装以及同源染色体重组相关蛋白的染色体定位均比较正常。
因此,OsHUS1参与了减数分裂过程中非同源重组的调控与抑制作用,并且这种作用很可能是以9-1-1复合体形式共同参与的。
该研究为探索同源重组的保障机制提供了先例,结果于2014年6月5日在PLoS genetics杂志上在线发表。相关研究得到科技部和国家自然科学基金委项目的资助。
原文摘要:
OsHUS1 Facilitates Accurate Meiotic Recombination in Rice
Lixiao Che, Kejian Wang, Ding Tang, Qiaoquan Liu equal contributor, Xiaojun Chen, Yafei Li, Qing Hu, Yi Shen, Hengxiu Yu, Minghong Gu, Zhukuan Cheng
Meiotic recombination normally takes place between allelic sequences on homologs. This process can also occur between non-allelic homologous sequences. Such ectopic interaction events can lead to chromosome rearrangements and are normally avoided. However, much remains unknown about how these ectopic interaction events are sensed and eliminated. In this study, using a screen in rice, we characterized a homolog of HUS1 and explored its function in meiotic recombination. In Oshus1 mutants, in conjunction with nearly normal homologous pairing and synapsis, vigorous, aberrant ectopic interactions occurred between nonhomologous chromosomes, leading to multivalent formation and subsequent chromosome fragmentation. These ectopic interactions relied on programed meiotic double strand breaks and were formed in a manner independent of the OsMER3-mediated interference-sensitive crossover pathway. Although early homologous recombination events occurred normally, the number of interference-sensitive crossovers was reduced in the absence of OsHUS1. Together, our results indicate that OsHUS1 might be involved in regulating ectopic interactions during meiosis, probably by forming the canonical RAD9-RAD1-HUS1 (9-1-1) complex.
作者:遗传发育所