| First Author | Leloup C | Year | 2010 |
| Journal | Dev Dyn | Volume | 239 |
| Issue | 11 | Pages | 2837-50 |
| PubMed ID | 20842695 | Mgi Jnum | J:165426 |
| Mgi Id | MGI:4837292 | Doi | 10.1002/dvdy.22415 |
| Citation | Leloup C, et al. (2010) Mouse Rad9b is essential for embryonic development and promotes resistance to DNA damage. Dev Dyn 239(11):2837-50 |
| abstractText | RAD9 participates in promoting resistance to DNA damage, cell cycle checkpoint control, DNA repair, apoptosis, embryogenesis, and regulation of transcription. A paralogue of RAD9 (named RAD9B) has been identified. To define the function of mouse Rad9b (Mrad9b), embryonic stem (ES) cells with a targeted gene deletion were constructed and used to generate Mrad9b mutant mice. Mrad9b(-/-) embryos are resorbed after E7.5 while some of the heterozygotes die between E12.5 and a few days after birth. Mrad9b is expressed in embryonic brain and Mrad9b(+/-) embryos exhibit abnormal neural tube closure. Mrad9b(-/-) mouse embryonic fibroblasts are not viable. Mrad9b(-/-) ES cells are more sensitive to gamma rays and mitomycin C than Mrad9b(+/+) controls, but show normal gamma-ray-induced G2/M checkpoint control. There is no evidence of spontaneous genomic instability in Mrad9b(-/-) cells. Our findings thus indicate that Mrad9b is essential for embryonic development and mediates resistance to certain DNA damaging agents. |
