{Models}
| Symbol: {Links}
|
Flybase ID: {Flybase_ID} |
| Synonyms: {Name}
|
{GadFly} |
| Function: {Short_Function} |
{LocusLink} |
| Keywords: {Keywords} |
{Interactive_Fly} |
{Summary}
|
- Sex-lethal (Sxl) is the sex determination master switch and it controls
somatic sexual development.
- Sxl is a splicing and translational regulator.
- "Sxl is activated in females where the X chromosome to autosome
(X:A) ratio is 1. It remains ‘off’ in males where the X:A
ratio is 0.5. Once set, these two modes of Sxl expression are maintained
through the rest of the life cycle (Sanchez and Nothiger, 1983; Cline,
1984). In females, a positive autoregulatory feedback loop that functions
through alternative splicing maintains the on state (Bell et al., 1991).
The male mode of splicing is maintained by default. Sxl directs somatic
sexual development by controlling the dosage compensation system (Lucchesi,
1978) and the somatic sexual differentiation pathway (reviewed by Cline
and Meyer, 1996). The dose compensation system is turned off by Sxl,
through both splicing regulation and translational repression (Bashaw
and Baker, 1997; Kelley et al., 1997). In somatic sexual development,
Sxl promotes female differentiation by controlling the female specific
splicing of the transformer gene (Boggs et al., 1987; McKeown et al.,
1987). The final requirement of Sxl is in oogenesis. Pole cell transplantation
experiments have demonstrated that female germ cells require Sxl for
regulating mitosis. Germ cells that lack Sxl develop as tumorous cysts
of many small undifferentiated cells (Schupbach, 1985), a phenotype
that is shared by the female sterile alleles of Sxl. Additionally, Sxl
regulates the splicing of its own transcripts (Hager and Cline,1997),
as well as the female-specific process of meiotic recombination (Schütt
et al., 1998; Bopp et al., 1999). The germline targets of Sxl are not
known, but they are not the somatic ones (Marsh and Wieschaus, 1978;
Schupbach, 1985)" (Vied,
2001)
- Vied,
2001 propose that g-tubulin together with Cos2, tether Sxl to microtubules
maintaining Sxl in the cytoplasm until Hh, or an effector of the Hh
signal, releases Sxl from the complex.
|
- Ptc and Fu in the germarium undergo changes in expression that are
coincident with Sxl (Vied,
2001)
|
- Immunoprecipitations from ovarian extracts show that Sxl is in a complex
with Fu and Cos2, along with b- and g-tubulin (Vied,
2001)
|