Rad54 is dispensable for the ALT pathway
Rad54 is dispensable for the ALT pathway
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DOI：
10.1111/j.1365-2443.2006.01020.x
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发表时间：
2006-11-01
期刊：
影响因子：
2.1
通讯作者：
Shinkai, Yoichi
中科院分区：
文献类型：
--
作者：
Akiyama, Koichi;Yusa, Kosuke;Shinkai, Yoichi
一些永生细胞使用替代端粒延长（ALT）途径来维持其端粒而不是端粒酶。以往的研究表明，同源重组（HR）有助于ALT途径。为了进一步阐明分子机制，我们在小鼠ALT胚胎干（ES）细胞中灭活了参与HR的Rad54。尽管Rad54缺陷型ALT ES细胞表现出与预期一致的放射敏感性，但细胞生长和端粒维持超过200次细胞分裂。此外，虽然MMC刺激的姐妹染色单体交换（SCE）被抑制在Rad54缺陷ALT ES细胞，ALT相关的端粒SCE不受影响。这是第一个遗传学证据表明小鼠Rad54是ALT途径的启动子。
Some immortal cells use the alternative lengthening of telomeres (ALT) pathway to maintain their telomeres instead of telomerase. Previous studies revealed that homologous recombination (HR) contributes to the ALT pathway. To further elucidate molecular mechanisms, we inactivated Rad54 involved in HR, in mouse ALT embryonic stem (ES) cells. Although Rad54-deficient ALT ES cells showed radiosensitivity in line with expectation, cell growth and telomeres were maintained for more than 200 cell divisions. Furthermore, although MMC-stimulated sister chromatid exchange (SCE) was suppressed in the Rad54-deficient ALT ES cells, ALT-associated telomere SCE was not affected. This is the first genetic evidence that mouse Rad54 is dispensable for the ALT pathway.