3'UTR has been truncated to remove 8 out of 10 of the putative Sxl binding sites.
Extra pole cells are evident in embryos derived from SxlFLΔ.Hsp83 mothers at all stages of development. Germ cells show migration defects, beginning at stage 10. Early defects include failure to contact gonadal mesoderm and premature clumping. Later phenotypes include lack of sustained contact with presumptive gonadal mesoderm and failure to coalesce. Germ cells can be small and irregularly shaped. These defects are not sex-specific.
Males are killed by a single copy of the P{Hsp83-Sxl.FLΔ-MS3} transgene. Male killing activity is greater than for the parental allele, SxlFL.Hsp83, but the effect is only revealed in particular genetic backgrounds, since the lethality caused by SxlFL.Hsp83 is complete. Male killing activity does not depend on a functional Sxl product.
SxlFLΔ.Hsp83 has phenotype, non-suppressible by msl-2Hsp83.PK
The few SxlFLΔ.Hsp83/SxlfP7B0 males rescued to viability by msl-2Hsp83.PK show intersex characteristics. They have lighter abdominal pigmentation, rotated genitalia, fewer sex combs and are sterile.
SxlFLΔ.Hsp83 partially rescues Sxlf2593
SxlFLΔ.Hsp83 partially rescues Sxlf7,M1
SxlFLΔ.Hsp83 fails to rescue SxlM1,f3
Rescue of Sxlf2593 by SxlFL.Hsp83 is more effective than that by SxlFLΔ.Hsp83 or SxlNΔ.Hsp83.