Rad54 is dispensable for the ALT pathway
| Autor: | Anuradha Poonepalli, Koichi Akiyama, Naoki Kakazu, Kosuke Yusa, Makoto Tachibana, Yoichi Shinkai, Junji Takeda, Manoor Prakash Hande, Hideharu Hashimoto |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Telomerase
Cell Sister chromatid exchange Biology digestive system Cell Line Mice Genetics medicine Animals Radiosensitivity Embryonic Stem Cells Mice Knockout Recombination Genetic Cell growth fungi DNA Helicases Nuclear Proteins Cell Biology Telomere Embryonic stem cell Molecular biology digestive system diseases medicine.anatomical_structure Homologous recombination Sister Chromatid Exchange Signal Transduction |
| Zdroj: | Genes to Cells. 11:1305-1315 |
| ISSN: | 1365-2443 1356-9597 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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