Premium
Mouse Rad9b is essential for embryonic development and promotes resistance to DNA damage
Author(s) -
Leloup Corinne,
Hopkins Kevin M.,
Wang Xiangyuan,
Zhu Aiping,
Wolgemuth Debra J.,
Lieberman Howard B.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22415
Subject(s) - biology , embryonic stem cell , dna damage , microbiology and biotechnology , embryogenesis , dna repair , cell cycle checkpoint , embryo , mitomycin c , genetics , genome instability , apoptosis , gene , cell cycle , dna
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. Developmental Dynamics 239:2837–2850, 2010. © 2010 Wiley‐Liss, Inc.