HTP-1-dependent constraints coordinate homolog pairing and synapsis and promote chiasma formation during C-elegans meiosis
HTP-1-dependent constraints coordinate homolog pairing and synapsis and promote chiasma formation during C-elegans meiosis
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DOI：
10.1101/gad.1338505
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发表时间：
2005-11-15
影响因子：
10.5
通讯作者：
Villeneuve, AM
中科院分区：
文献类型：
--
作者：
Martinez-Perez, E;Villeneuve, AM
联会复合体（SC）的装配必须发生在正确配对的同源染色体之间，以促进交叉的形成。在这里，我们确定秀丽隐杆线虫HORMA结构域蛋白HTP-1作为协调建立同源配对和突触在C。elegans和提供的证据，检查点样机制耦合这些早期减数分裂前期事件。htp-1突变体在配对的建立上是有缺陷的，但与配对缺陷的chk-2突变体相反，SC组装不受抑制，并且发生广义的非同源突触。广泛的非同源性突触在htp-1，chk-2双突变体表明，HTP-1所需的抑制SC组装观察chk-2性腺。htp-1突变体显示出显示极化组织的核的丰度降低，极化组织通常伴随配对的建立;对htp-1; syp-2双突变体的分析表明，需要HTP-1来防止过早退出这种极化的核组织，并且这种退出停止同源性搜索。此外，基于监测重组中间体和交叉产物形成的实验，我们认为htp-1突变体在阻止使用姐妹染色单体作为重组伴侣方面存在缺陷。我们提出了一个模型，其中HTP-1的功能，以建立或维护多个约束，操作，以确保协调的事件导致交叉形成。
Synaptonemal complex (SC) assembly must occur between correctly paired homologous chromosomes to promote formation of chiasmata. Here, we identify the Caenorhabditis elegans HORMA-domain protein HTP-1 as a key player in coordinating establishment of homolog pairing and synapsis in C. elegans and provide evidence that checkpoint-like mechanisms couple these early meiotic prophase events. htp-1 mutants are defective in the establishment of pairing, but in contrast with the pairing-defective chk-2 mutant, SC assembly is not inhibited and generalized nonhomologous synapsis occurs. Extensive nonhomologous synapsis in htp-1; chk-2 double mutants indicates that HTP-1 is required for the inhibition of SC assembly observed in chk-2 gonads. htp-1 mutants show a decreased abundance of nuclei exhibiting a polarized organization that normally accompanies establishment of pairing; analysis of htp-1; syp-2 double mutants suggests that HTP-1 is needed to prevent premature exit from this polarized nuclear organization and that this exit stops homology search. Further, based on experiments monitoring the formation of recombination intermediates and crossover products, we suggest that htp-1 mutants are defective in preventing the use of sister chromatids as recombination partners. We propose a model in which HTP-1 functions to establish or maintain multiple constraints that operate to ensure coordination of events leading to chiasma formation.