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首页> 外文期刊>Developmental cell >The Fidelity of Synaptonemal Complex Assembly Is Regulated by a Signaling Mechanism that Controls Early Meiotic Progression.
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The Fidelity of Synaptonemal Complex Assembly Is Regulated by a Signaling Mechanism that Controls Early Meiotic Progression.

机译：联会复杂装配的保真度受控制早期减数分裂进程的信号传导机制调控。

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摘要

Proper chromosome segregation during meiosis requires the assembly of the synaptonemal complex (SC) between homologous chromosomes. However, the SC structure itself is indifferent to homology, and?poorly understood mechanisms that depend on conserved HORMA-domain proteins prevent ectopic SC assembly. Although HORMA-domain proteins are thought to regulate SC assembly as intrinsic components of meiotic chromosomes, here we uncover a key role for nuclear soluble HORMA-domain protein HTP-1 in the quality control of SC assembly. We show that a mutant form of HTP-1 impaired in chromosome loading provides functionality of an HTP-1-dependent checkpoint that delays exit from homology search-competent stages until all homolog pairs are linked by the SC. Bypassing of this regulatory mechanism results in premature meiotic progression and licensing of homology-independent SC assembly. These findings identify nuclear soluble HTP-1 as a regulator of early meiotic progression, suggesting parallels with the mode of action of Mad2 in the spindle assembly checkpoint.
机译：减数分裂过程中正确的染色体分离需要同源染色体之间的突触复合体（SC）的组装。然而，SC结构本身对同源性无动于衷，并且依赖于保守的HORMA域蛋白的人们普遍了解的机制阻止了异位SC的组装。尽管HORMA域蛋白被认为调节SC组装作为减数分裂染色体的固有成分，但在这里我们揭示了核可溶性HORMA域蛋白HTP-1在SC组装质量控制中的关键作用。我们表明，在染色体加载中受损的HTP-1突变形式提供了HTP-1依赖检查点的功能，该功能延迟从同源搜索胜任阶段的退出，直到所有同源物对均由SC链接。绕过该调节机制导致过早的减数分裂进程和不依赖同源性的SC组装的许可。这些发现确定了核可溶性HTP-1是早期减数分裂进程的调节剂，表明与纺锤体装配检查点中Mad2的作用方式相似。

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