ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis
ASY1 mediates AtDMC1-dependent interhomolog recombination during meiosis in Arabidopsis
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DOI：
10.1101/gad.439007
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发表时间：
2007-09-01
影响因子：
10.5
通讯作者：
Franklin, F. Christopher H.
中科院分区：
文献类型：
--
作者：
Sanchez-Moran, Eugenio;Santos, Juan-Luis;Franklin, F. Christopher H.
ASY1是拟南芥的一种蛋白质，在减数分裂过程中需要进行突触和交叉形成。对野生型和asy1突变体的减数分裂重组年表进行了研究。我们观察到染色质相关的AtSPO11-1焦点的出现和DNA双链断裂(DSB)的形成之间存在延迟，这与染色体轴的形成和ASY1从染色质相关焦点到线性轴相关信号的转变同时发生。DSB以AtSPO11-1依赖的方式独立于ASY1形成。使用顺铂可以部分恢复ATSP11-1-3中的它们，但它们的控制似乎不正常。轴的形态发生与ASY1无关，但在ASY1中轴的结构可能受到影响。链交换蛋白AtRAD51和AtDMC1在DSB形成后不久就异步定位到染色质，AtDMC1先于AtRAD51定位。在野生型细胞核中，两种重组酶形成大量的焦点，这些焦点持续-12小时，然后逐渐减少。在asy1中，AtDMC1的初始定位是正常的，但突然下降，导致同源重组严重受损。有限的ASY1非依赖的、DMC1依赖的同源基因间重组仍然存在，但似乎仅限于亚端粒序列，其中同源基因偶然接近。因此，ASY1在协调RecA同源物的活性以创造有利于同源物间重组的偏向方面发挥了关键作用。
ASY1 is an Arabidopsis protein required for synapsis and crossover formation during meiosis. The chronology of meiotic recombination has been investigated in wild type and an asy1 mutant. We observe a delay between the appearance of chromatin-associated AtSPO11-1 foci and DNA double-strand break (DSB) formation, which occurs contemporaneously with chromosome axis formation and transition of ASY1 from chromatin-associated foci to a linear axis-associated signal. DSBs are formed independently of ASY1 in an AtSPO11-1-dependent manner. They are partially restored in Atspo11-1-3 using cisplatin, but their control appears abnormal. Axis morphogenesis is independent of ASY1, but axis structure may be compromised in asy1. Localization of the strand exchange proteins AtRAD51 and AtDMC1 to the chromatin occurs asynchronously shortly after DSB formation, with AtDMC1 localizing in advance of AtRAD51. In wild-type nuclei, both recombinases form numerous foci that persist for -12 h before gradually decreasing in number. In asy1, initial localization of AtDMC1 is normal, but declines abruptly such that interhomolog recombination is severely compromised. Limited ASY1-independent, DMC1-dependent interhomolog recombination remains, but appears restricted to subtelomeric sequences where the homologs are fortuitously in proximity. Thus, ASY1 plays a key role in coordinating the activity of the RecA homologs to create a bias in favor of interhomolog recombination.