Alleles of afd1 dissect REC8 functions during meiotic prophase I
Alleles of afd1 dissect REC8 functions during meiotic prophase I
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DOI：
10.1242/jcs.03054
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发表时间：
2006-08-15
影响因子：
4
通讯作者：
Cande, W. Zacheus
中科院分区：
文献类型：
--
作者：
Golubovskaya, Inna N.;Hamant, Olivier;Cande, W. Zacheus
REC8 是减数分裂过程中染色质结构和功能的主要调节因子。在这里，我们使用独特的 afd1 等位基因系列剖析了缺乏第一分裂 (afd1)（玉米 rec8/alpha-kleisin 同源物）的功能。 afd1 突变体中第一个可观察到的缺陷是无法形成细线染色体。 AFD1 蛋白是轴向元件伸长所必需的，但其初始募集则不需要，因此表明 AFD1 作用于 ASY1/HOP1 下游。 AFD1 与联会复合体的轴向元件以及随后的横向元件相关。在最弱的 afd1 等位基因中挽救 50% 的轴向元件伸长恢复了花束形成，表明端粒聚类的程度取决于轴向元件伸长。然而，拯救花束的形成对于正确的 RAD51 分布或同源配对来说是不够的。它为模型提供了基础，在该模型中，AFD1/REC8 通过其在轴向元件伸长中的作用以及独立于花束形成的重组机制的后续分布来控制同源配对。
REC8 is a master regulator of chromatin structure and function during meiosis. Here, we dissected the functions of absence of first division (afd1), a maize rec8/alpha-kleisin homolog, using a unique afd1 allelic series. The first observable defect in afd1 mutants is the inability to make a leptotene chromosome. AFD1 protein is required for elongation of axial elements but not for their initial recruitment, thus showing that AFD1 acts downstream of ASY1/HOP1. AFD1 is associated with the axial and later the lateral elements of the synaptonemal complex. Rescuing 50% of axial element elongation in the weakest afd1 allele restored bouquet formation demonstrating that extent of telomere clustering depends on axial element elongation. However, rescuing bouquet formation was not sufficient for either proper RAD51 distribution or homologous pairing. It provides the basis for a model in which AFD1/REC8 controls homologous pairing through its role in axial element elongation and the subsequent distribution of the recombination machinery independent of bouquet formation.