Rad54 is dispensable for the ALT pathway

被引：7

作者：

Akiyama, Koichi

Yusa, Kosuke

Hashimoto, Hideharu

Poonepalli, Anuradha

Prakash Hande, Manoor

Kakazu, Naoki

Takeda, Junji

Tachibana, Makoto

Shinkai, Yoichi

机构：

[1] Kyoto Univ, Grad Sch Biostudies, Dept Life Sci, Sakyo Ku, Kyoto 6068507, Japan

[2] Kyoto Univ, Expt Res Ctr Infect Dis, Inst Virus Res, Sakyo Ku, Kyoto 6068507, Japan

[3] Osaka Univ, Grad Sch Med, Dept Social & Environm Med, Suita, Osaka 5650871, Japan

[4] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117597, Singapore

[5] Shimane Univ, Sch Med, Dept Environm & Prevent Med, Izumo, Shimane 6938501, Japan

来源：

GENES TO CELLS | 2006年 / 11卷 / 11期

关键词：

D O I：

10.1111/j.1365-2443.2006.01020.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：1305 / 1315

页数：11

共 44 条

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