Not associated with any gross DNA change. Based on recombination mapping and conversion factor of 1μMorgan=47bp (based on FBrf0042060), the Sxlf9 lesion maps approximately 3.3kb downstream of the SxlM1 lesion.
Probably point mutation (no gross alteration in DNA).
Defective in some very early steps in the sex-determination process, but which has no adverse effect on the growth or sexual development of homozygous mutant diplo-X clones induced by mitotic recombination. Rare escapers at 18oC are phenotypically female; nevertheless, it has a dominant masculinizing effect on the phenotype of triploid intersexes ( 2X:3A ) and interacts in a dominant-lethal fashion with mutations in da or sisA, both early acting positive regulators of Sxl. Fully complements "SxlfPR" class (partial deletions of Sxl information that impair later functions of the gene more than earlier).
Fully complements SxlfLS.
Sxlf9 is a non-suppressor of decreased fecundity | dominant | female phenotype of ovoD2
Sxl[+]/Sxlf9, msl-31 has lethal | female | maternal effect phenotype
Sxlf9, fl(1)3535 has partially lethal | female phenotype
Sxlf9, fl(1)3546 has partially lethal | female phenotype
Sxlf9, l(1)4343 has partially lethal | female phenotype
SxlF1.hs can rescue 40% female lethality and the survivors are fertile.
Sxlf9 fully complements SxlM1,f3. Complements SxlfLS and Sxlf2, and partially complements Sxlf7,M1 for female viability. Recombination distance between Sxlf9 and 'f3' of SxlM1,f3 is 0.015cM. Recombination distance between Sxlf9 and SxlM1 is 0.007cM.
Defective in the initiation of Sxl function.