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Rad54 is dispensable for the ALT pathway
Author(s) -
Akiyama Koichi,
Yusa Kosuke,
Hashimoto Hideharu,
Poonepalli Anuradha,
Hande Manoor Prakash,
Kakazu Naoki,
Takeda Junji,
Tachibana Makoto,
Shinkai Yoichi
Publication year - 2006
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2006.01020.x
Subject(s) - biology , telomere , telomerase , embryonic stem cell , microbiology and biotechnology , sister chromatid exchange , homologous recombination , genetics , dna , gene
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.