| First Author | Qiao H | Year | 2018 |
| Journal | Mol Cell | Volume | 72 |
| Issue | 2 | Pages | 211-221.e3 |
| PubMed ID | 30270110 | Mgi Jnum | J:268828 |
| Mgi Id | MGI:6270033 | Doi | 10.1016/j.molcel.2018.08.031 |
| Citation | Qiao H, et al. (2018) Impeding DNA Break Repair Enables Oocyte Quality Control. Mol Cell 72(2):211-221.e3 |
| abstractText | Oocyte quality control culls eggs with defects in meiosis. In mouse, oocyte death can be triggered by defects in chromosome synapsis and recombination, which involve repair of DNA double-strand breaks (DSBs) between homologous chromosomes. We show that RNF212, a SUMO ligase required for crossing over, also mediates oocyte quality control. Both physiological apoptosis and wholesale oocyte elimination in meiotic mutants require RNF212. RNF212 sensitizes oocytes to DSB-induced apoptosis within a narrow window as chromosomes desynapse and cells transition into quiescence. Analysis of DNA damage during this transition implies that RNF212 impedes DSB repair. Consistently, RNF212 is required for HORMAD1, a negative regulator of inter-sister recombination, to associate with desynapsing chromosomes. We infer that oocytes impede repair of residual DSBs to retain a "memory" of meiotic defects that enables quality-control processes. These results define the logic of oocyte quality control and suggest RNF212 variants may influence transmission of defective genomes. |
