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PLoS Gene:程祝宽等同源重组机制研究获进展

来源:中科院遗传发育所 2012-07-13 22:26

减数分裂是维持生物体染色体数恒定,导致遗传重组产生的基础。减数分裂缺陷是导致不孕、不育和出生障碍的主要原因。绝大多数减数分裂基因在不同物种中有着高度保守的功能。HEI10基因最初在人类体细胞中分离,并证明有调控细胞周期的功能。在小鼠中研究表明HEI10基因的突变会导致减数分裂异常并最终导致不育,但是HEI10在减数分裂过程中的具体生物学功能目前仍然不清楚。
 
程祝宽课题组在水稻中鉴定出了HEI10基因,研究分析发现HEI10基因突变导致交叉结的数目显著减少,而剩余交叉随机分布于不同染色体上。但是HEI10的突变并不影响重组早期蛋白的定位以及联会复合体的形成。令人惊奇的是,HEI10蛋白在染色体上呈现一种动态的定位:最初呈现为明显的点状而且与重组蛋白MER3高度共定位,随着减数分裂联会的进行,HEI10沿着染色体轴逐渐连成线状信号,在联会复合体解体之后,线状信号逐渐消失,只有大的点状信号维持在染色体上,而这些点状信号恰好对应于交叉结的位置。HEI10是水稻中分离的第一个可以用于指示重组位置的标记蛋白,相关研究为在水稻中进一步深入研究重组机制提供了坚实基础。
 
该研究结果于2012年7月5日在线发表于PLoS Genetics杂志上,程祝宽实验室王克剑、王莫和唐丁为该工作的共同第一作者。该项工作受到科技部及国家自然科学基金委项目的资助。(生物谷Bioon.com)

The Role of Rice HEI10 in the Formation of Meiotic Crossovers

Kejian Wang1#, Mo Wang1#, Ding Tang1#, Yi Shen1, Chunbo Miao1, Qing Hu1, Tiegang Lu2, Zhukuan Cheng1*

HEI10 was first described in human as a RING domain-containing protein that regulates cell cycle and cell invasion. Mice HEI10mei4 mutant displays no obvious defect other than meiotic failure from an absence of chiasmata. In this study, we characterize rice HEI10 by map-based cloning and explore its function during meiotic recombination. In the rice hei10 mutant, chiasma frequency is markedly reduced, and those remaining chiasmata exhibit a random distribution among cells, suggesting possible involvement of HEI10 in the formation of interference-sensitive crossovers (COs). However, mutation of HEI10 does not affect early recombination events and synaptonemal complex (SC) formation. HEI10 protein displays a highly dynamic localization on the meiotic chromosomes. It initially appears as distinct foci and co-localizes with MER3. Thereafter, HEI10 signals elongate along the chromosomes and finally restrict to prominent foci that specially localize to chiasma sites. The linear HEI10 signals always localize on ZEP1 signals, indicating that HEI10 extends along the chromosome in the wake of synapsis. Together our results suggest that HEI10 is the homolog of budding yeast Zip3 and Caenorhabditis elegans ZHP-3, and may specifically promote class I CO formation through modification of various meiotic components.

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