Approximately 20% of Sxlf2 mutant germaria contain cystoblasts with defects in differentiation.
Sexual differentiation of external adult tissues in heteroallelic escaper females carrying SxlfPRJ2 or SxlfLS is normal. Sexual differentiation of homozygous escaper females is also normal, as is the differentiation of clones of homozygous Sxlf2 tissue in a heterozygous background. Nonetheless escaper females have rudimentary gonads that are covered with testes sheath tissue. SxlfPRJ2/Sxlf1 shows wild type dosage compensation in run25 phenotype assay.
Some escaper adult females.
Homozygous females are either inviable or very poorly viable, depending on genetic background. Escapers are invariably sterile but otherwise display no obvious sexual abnormalities. Homozygotes defective in dosage compensation as indicated by hyperincorporation of uridine by their polytene chromosomes. Allele fails to support oogenesis in germ-line clones induced by mitotic recombination.
Sxlf2 is a non-suppressor of decreased fecundity | dominant | female phenotype of ovoD2
Sxlf4/Sxlf2, otu17 has female sterile | dominant phenotype
Sxlf2, mle4 has abnormal sex-determination | dominant | female phenotype
Sxlf2, mle4 has abnormal sex-determination | female phenotype
Sxlf2, mle4 has prothoracic metatarsus | female phenotype
Zimmering and Muller, 1961.
Complements Sxlf9, and partially complements SxlfLS, Sxlf7,M1 and Sxlf2 for female viability. Defective in Sxl Pm-mediated activities - the later functions governing maintenance and expression of the female-committed developmental state. Autoregulatory activity involved in maintaining the female determined state is wild type for external somatic tissues, as assayed by interaction with snf.