Mammalian Fbh1 is important to restore normal mitotic progression following decatenation stress.

ABSTRACT: We have addressed the role of the F-box helicase 1 (Fbh1) protein during genome maintenance in mammalian cells. For this, we generated two mouse embryonic stem cell lines deficient for Fbh1: one with a homozygous deletion of the N-terminal F-box domain (Fbh1(f/f)), and the other with a homozygous disruption (Fbh1(-/-)). Consistent with previous reports of Fbh1-deficiency in vertebrate cells, we found that Fbh1(-/-) cells show a moderate increase in Rad51 localization to DNA damage, but no clear defect in chromosome break repair. In contrast, we found that Fbh1(f/f) cells show a decrease in Rad51 localization to DNA damage and increased cytoplasmic localization of Rad51. However, these Fbh1(f/f) cells show no clear defects in chromosome break repair. Since some Rad51 partners and F-box-asso

SUBMITTER: Laulier C 

PROVIDER: S-EPMC2883650 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature