It has previously been shown that germ cells in embryos derived from nos mutant mothers do not migrate to the primitive gonad and prematurely express several germline-specific markers. In the studies reported here, we have traced these defects back to the syncytial blastoderm stage. We show that pole cells in nos- embryos fail to establish/maintain transcriptional quiescence; the sex determination gene Sex-lethal (Sxl) and the segmentation genes fushi tarazu and even-skipped are ectopically activated in nos- germ cells. We show that nos- germ cells are unable to attenuate the cell cycle and instead continue dividing. Unexpectedly, removal of the Sxl gene in the zygote mitigates both the migration and mitotic defects of nos- germ cells. Supporting the conclusion that Sxl is an important target for nos repression, ectopic, premature expression of Sxl protein in germ cells disrupts migration and stimulates mitotic activity.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Oct 29 1999|
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)