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Genes to Cells (2006) 11, 1305-1315. doi:10.1111/j.1365-2443.2006.01020.x
© 2006 Blackwell Publishing or its licensors
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Rad54 is dispensable for the ALT pathway

Koichi Akiyama1,2, Kosuke Yusa3, Hideharu Hashimoto1,2, Anuradha Poonepalli4, Manoor Prakash Hande4, Naoki Kakazu5, Junji Takeda3, Makoto Tachibana1,2 and Yoichi Shinkai1,2,*

1 Department of Life Science, Graduate School of Biostudies;
2 Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Kawara-cho, Shogoin, Sakyo-ku, Kyoto Kyoto 606-8507, Japan
3 Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan
4 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Block MD9, 2 Medical Drive, Singapore 117597, Singapore
5 Department of Environmental and Preventive Medicine, Shimane University School of Medicine, 89-1 Enya-cho, Izumo Shimane 693-8501, Japan

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.

Communicated by: Fuyuki Ishikawa

* Correspondence: E-mail: yshinkai{at}virus.kyoto-u.ac.jp






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