| Print Close window |
| Session Information |
|---|
| Session Title: Organogenesis and Gametogenesis Session Type: Poster |
| Session Location: Grand Exhibit Hall Session Time: Thursday - Saturday |
| Presentation Information |
| Poster Board Number: 507C Presentation Time: THU 3:00PM-4:00PM, 10:00PM-11:00PM; FRI 8:00PM-9:00PM; SAT 1:30PM-2:30PM; |
| Keywords: KW07e - stem cells |
| Presentation Content |
|
Sex-lethal is required for asymmetric fate specification of ovarian germ cells. Johnnie Chau, Laura Shapiro Kulnane, Helen K. Salz. Department of Genetics, Case Western Reserve University, Cleveland, OH. Sex-lethal (Sxl) encodes a female-specific RNA binding protein that is the "master regulator" of sexual cell fate in the soma. Sxl is also required for ovarian germ cell development, but its role remains unclear. Here, we characterized the snf148 ovarian tumor phenotype, which is due solely to the absence of SXL in the germline. The snf mutant ovary accumulates proliferating germ cells with abnormal fusome-like structures of varying shapes. Nevertheless, our analysis of both snf, CycB and snf, zpg double mutants indicates that the tumor cells continue to require at least some of the same essential growth-control mechanisms used by wild type germ cells. Interestingly, we find that in tumor cells the distinction between germline stem cells (GSCs) and the mitotic cyst cells is disrupted. Normally, the transition from GSC to its differentiated daughter cell requires the coincident down regulation of piwi and pum, two GSC self-renewal genes, with the upregulation of bam, a differentiation gene. Following the expression of these molecular markers, we show that the proliferating snf tumor cells express all three molecular markers. In particular, we detect bam expression in the most apical tumor cells where transcription is normally repressed by dpp signaling. Because snf tumor cells can receive dpp signals, as assayed by activation of a dad-lacZ reporter construct, we propose that SXL functions in the GSCs to interpret (either directly or indirectly) the signals that silence bam transcription. Our observation that precocious BAM expression is not sufficient to drive differentiation in a snf mutant background, combined with the phenotype of snf, bam double mutants, indicates that SXL is also required for BAM protein function. In summary, our data lead to a model in which at least two different programming events required for asymmetric cell fate specification in the germline are under Sxl control. Studies to understand the molecular mechanism by which SXL controls these pathways are underway. |
| Print Close window |