| First Author | Odorisio T | Year | 1998 |
| Journal | Nat Genet | Volume | 18 |
| Issue | 3 | Pages | 257-61 |
| PubMed ID | 9500548 | Mgi Jnum | J:46385 |
| Mgi Id | MGI:1197802 | Doi | 10.1038/ng0398-257 |
| Citation | Odorisio T, et al. (1998) The meiotic checkpoint monitoring synapsis eliminates spermatocytes via p53-independent apoptosis [see comments]. Nat Genet 18(3):257-61 |
| abstractText | Evidence is accumulating that meiosis is subject to 'checkpoints' that monitor the quality of this complex process. In yeast, unresolved double strand breaks (DSBs) in DNA are thought to trigger a 'recombination checkpoint' that leads to pachytene arrest. In higher eukaryotes, there is evidence for a checkpoint that monitors chromosome synapsis and in mammals the most compelling evidence relates to the sex chromosomes. In normal male mice, there is synapsis between the X and Y pseudoautosomal regions; in XSxr(a)O mice, with a single asynaptic sex chromosome, there is arrest at the first meiotic metaphase, the arrested cells being eliminated by apoptosis (our unpublished data). Satisfying the requirement for pseudoautosomal synapsis by providing a pairing partner for the XSxr(a) chromosome avoids this arrest. We have considered that this 'synapsis checkpoint' may be a modification of the yeast 'recombination checkpoint' with unresolved DSBs (a corollary of asynapsis) providing the trigger for apoptosis. DSBs induced by irradiation are known to trigger apoptosis in a number of cell types via a p53-dependent pathway, and we now show that irradiation-induced spermatogonial apoptosis is also p53-dependent. In contrast, the apoptotic elimination of spermatocytes with synaptic errors proved to be p53-independent. |
