Failure of homologous synapsis and sex-specific reproduction problems.

Failure of homologous synapsis and sex-specific reproduction problems.
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DOI:
10.3389/fgene.2012.00112
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发表时间:
2012
影响因子:
3.7
通讯作者:
Ohye T
Ohye T
中科院分区:
生物学3区
文献类型:
--
作者:
Kurahashi H;Kogo H;Tsutsumi M;Inagaki H;Ohye T

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减数分裂I的前期确保染色体正确地分离到每个子细胞。这包括同源染色体的配对、联会和重组。染色体异常的一个子集,包括易位和倒位,扰乱了这些过程,导致无法完成突触。这激活了减数分裂粗线期检查点,配子注定要经历细胞周期停滞和随后的凋亡。生精细胞似乎更容易受到粗线期检查点的影响,染色体异常的男性携带者更容易不育。相比之下,卵母细胞往往绕过检查点,而是产生其他问题,如染色体不平衡,往往导致女性携带者反复流产。遗传操作技术的最新进展增加了我们对检测染色体突触的粗线期检查点和监视系统的了解。本文综述了人类突触失败的后果,并概述了所涉及的机制。我们还讨论了性二态性的参与途径,导致男性和女性之间的生殖结果的差异。
The prophase of meiosis I ensures the correct segregation of chromosomes to each daughter cell. This includes the pairing, synapsis, and recombination of homologous chromosomes. A subset of chromosomal abnormalities, including translocation and inversion, disturbs these processes, resulting in the failure to complete synapsis. This activates the meiotic pachytene checkpoint, and the gametes are fated to undergo cell cycle arrest and subsequent apoptosis. Spermatogenic cells appear to be more vulnerable to the pachytene checkpoint, and male carriers of chromosomal abnormalities are more susceptible to infertility. In contrast, oocytes tend to bypass the checkpoint and instead generate other problems, such as chromosome imbalance that often leads to recurrent pregnancy loss in female carriers. Recent advances in genetic manipulation technologies have increased our knowledge about the pachytene checkpoint and surveillance systems that detect chromosomal synapsis. This review focuses on the consequences of synapsis failure in humans and provides an overview of the mechanisms involved. We also discuss the sexual dimorphism of the involved pathways that leads to the differences in reproductive outcomes between males and females.
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