Rad54 is dispensable for the ALT pathway.
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.
Akiyama
Koichi
K
Department of Life Science, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Yusa
Kosuke
K
Hashimoto
Hideharu
H
Poonepalli
Anuradha
A
Hande
Manoor Prakash
MP
Kakazu
Naoki
N
Takeda
Junji
J
Tachibana
Makoto
M
Shinkai
Yoichi
Y
D000818:Animals; D002460:Cell Line; D004265:DNA Helicases; D053595:Embryonic Stem Cells / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009687:Nuclear Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D011995:Recombination, Genetic; D015398:Signal Transduction; D012854:Sister Chromatid Exchange; D016615:Telomere / Q000378:metabolism*
D009687:Nuclear Proteins; D004265:DNA Helicases; C103534:Rad54l protein, mouse