小鼠MutS样蛋白Msh5是雄性和雌性减数分裂中正确染色体联会所必需的。
Mouse MutS-like protein Msh5 is required for proper chromosome synapsis in male and female meiosis.
作者信息
de Vries S S, Baart E B, Dekker M, Siezen A, de Rooij D G, de Boer P, te Riele H
机构信息
Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
出版信息
Genes Dev. 1999 Mar 1;13(5):523-31. doi: 10.1101/gad.13.5.523.
Abstract
Members of the mammalian mismatch repair protein family of MutS and MutL homologs have been implicated in postreplicative mismatch correction and chromosome interactions during meiotic recombination. Here we demonstrate that mice carrying a disruption in MutS homolog Msh5 show a meiotic defect, leading to male and female sterility. Histological and cytological examination of prophase I stages in both sexes revealed an extended zygotene stage, characterized by impaired and aberrant chromosome synapsis, that was followed by apoptotic cell death. Thus, murine Msh5 promotes synapsis of homologous chromosomes in meiotic prophase I.
摘要
哺乳动物MutS和MutL同源物错配修复蛋白家族的成员参与了减数分裂重组过程中的复制后错配校正和染色体相互作用。在此，我们证明携带MutS同源物Msh5基因破坏的小鼠表现出减数分裂缺陷，导致雄性和雌性不育。对两性减数分裂前期I阶段的组织学和细胞学检查显示，偶线期延长，其特征是染色体联会受损和异常，随后是凋亡性细胞死亡。因此，小鼠Msh5促进减数分裂前期I同源染色体的联会。
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