Abstract:
Telomeres are located at the ends of linear chromosomes and play a critical role in maintaining genomic stability by preventing premature activation of DNA repair mechanisms. Because of exposure to various genotoxic agents, telomeres can undergo shortening and genetic changes. In mammalian cells, the basic DNA repair mechanisms, including base excision repair, nucleotide excision repair, double-strand break repair, and mismatch repair, function in repairing potential damages in telomeres. If these damages are not repaired correctly in time, the unfavorable results such as apoptosis, cell cycle arrest, and cancerous transition may occur. During lifespan, mammalian somatic cells, male and female germ cells, and preimplantation embryos experience a number of telomeric damages. Herein, we comprehensively reviewed the crosstalk between telomeres and the DNA repair mechanisms in the somatic cells, germ cells, and embryos. Infertility development resulting from possible defects in this crosstalk is also discussed in the light of existing studies.
摘要:
端粒位于线性染色体的末端,通过防止DNA修复机制的过早激活,在维持基因组稳定性中起关键作用。因为暴露于各种基因毒性因子,端粒可以经历缩短和遗传变化。在哺乳动物细胞中,基本的DNA修复机制,包括基底切除修复,核苷酸切除修复,双股断裂修复,和失配修复,修复端粒潜在损害的功能。如果这些损坏没有及时正确修复,不利的结果,如细胞凋亡,细胞周期停滞,可能会发生癌变。在寿命期间,哺乳动物体细胞,男性和女性生殖细胞,和植入前胚胎经历了许多端粒损伤。在这里,我们全面回顾了端粒之间的串扰和体细胞中的DNA修复机制,生殖细胞,和胚胎。根据现有研究,还讨论了由于这种串扰可能存在缺陷而导致的不育发展。