Hodges Craig A, Revenkova Ekaterina, Jessberger Rolf, Hassold Terry J, Hunt Patricia A
Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Nat Genet. 2005 Dec;37(12):1351-5. doi: 10.1038/ng1672. Epub 2005 Oct 30.
Mitotic chromosome segregation is facilitated by the cohesin complex, which maintains physical connections between sister chromatids until anaphase. Meiotic cell division is considerably more complex, as cohesion must be released sequentially to facilitate orderly segregation of chromosomes at both meiosis I and meiosis II. This necessitates meiosis-specific cohesin components; recent studies in rodents suggest that these influence chromosome behavior during both cell division and meiotic prophase. To elucidate the role of the meiosis-specific cohesin SMC1beta (encoded by Smc1l2) in oogenesis, we carried out meiotic studies of female SMC1beta-deficient mice. Our results provide the first direct evidence that SMC1beta acts as a chiasma binder in mammals, stabilizing sites of exchange until anaphase. Additionally, our observations support the hypothesis that deficient cohesion is an underlying cause of human age-related aneuploidy.
有丝分裂染色体分离由黏连蛋白复合体促进,该复合体维持姐妹染色单体之间的物理连接直至后期。减数分裂细胞分裂要复杂得多,因为黏连必须依次释放,以促进减数分裂I和减数分裂II中染色体的有序分离。这就需要减数分裂特异性黏连蛋白成分;最近在啮齿动物中的研究表明,这些成分会影响细胞分裂和减数分裂前期的染色体行为。为了阐明减数分裂特异性黏连蛋白SMC1β(由Smc1l2编码)在卵子发生中的作用,我们对雌性SMC1β缺陷小鼠进行了减数分裂研究。我们的结果提供了首个直接证据,表明SMC1β在哺乳动物中作为交叉结合蛋白,稳定交换位点直至后期。此外,我们的观察结果支持了以下假设,即黏连缺陷是人类年龄相关非整倍体的一个根本原因。