Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutants.

ABSTRACT: Defects in meiotic recombination in many organisms result in arrest because of activation of a meiotic checkpoint(s). The proximal defect that triggers this checkpoint in mammalian germ cells is not understood, but it has been suggested to involve either the presence of DNA damage in the form of unrepaired recombination intermediates or defects in homologous chromosome pairing and synapsis independent of DNA damage per se. To distinguish between these possibilities in the female germ line, we compared mouse oocyte development in a mutant that fails to form the double-strand breaks (DSBs) that initiate meiotic recombination (Spo11-/-) to mutants with defects in processing DSBs when they are formed (Dmc1-/- and Msh5-/-), and we examined the epistasis relationships between these mutations. Ab

SUBMITTER: Di Giacomo M 

PROVIDER: S-EPMC545532 | biostudies-literature | 2005 Jan

REPOSITORIES: biostudies-literature