Very few zfh175.26 mutant cyst progenitor cell clones are recovered compared to controls. The mutant cyst progenitor cells that are recovered have begun to express differentiation markers. Germline stem cell clones are recovered at similar levels to controls.
zfh15 and zfh15/zfh175.26 embryos show defects in the formation of ventral motor nerves. The ISN nerve is always present in these mutants but has branching defects. This nerve exits the CNS, but the ISNb and SNa nerves are truncated or absent. The SNc and ISNd nerves are not identifiable in these mutant embryos and it may be that the CNS stops developing before the formation of these minor nerves.
In male stage 13 embryos double mutant for zfh175.26 and Df(3R)GC14, male-specific somatic gonadal precursors are still specified, even though the somatic gonadal precursors fail to develop in parasegment 10-12.
Mutant embryos have mild defects in the development of the tracheal dorsal trunk.
Germ cells in mutant embryos do not successfully navigate to the somatic gonadal precursors (SGPs): the majority of the germ cells do not attach to the SGPs at stage 11. Germ cells migrate past their target mesodermal cells, into posterior or ectodermal regions. Occasionally small gonads may form. Embryos derived from homozygous germline clones develop normally as long as a wild-type copy of zfh1 is zygotically provided. The germ cell migration phenotype is not exacerbated when the embryos are derived from a zfh1 homozygous mutant germline. Germ cells are unable to transfer between germ layers in double mutant embryos with tin (Df(3R)GC14). Most germ cells adhere to the endoderm throughout embryogenesis, some scatter near the gut at late stages.
zfh175.26 has embryonic/larval tracheal dorsal trunk phenotype, enhanceable by tinEC40
zfh175.26 is an enhancer of embryonic/larval tracheal dorsal trunk phenotype of tinEC40
Df(3R)GC14, zfh175.26 has primordial germ cell phenotype
Df(3R)GC14, zfh175.26 has gonadal sheath proper primordium phenotype
Df(3R)GC14, zfh175.26 has fat body/gonad primordium phenotype
Pole cells occasionally aggregate and form pseudo-gonads at the level of the fifth abdominal segment in zfh175.26 Df(3R)GC14 double mutant embryos.
The addition of tinEC40 to mutants leads to a tracheal dorsal trunk that is almost completely absent.
zfh175.26; Df(3R)GC14 double mutant embryos completely lack gonadal mesoderm, and the number of fat body precursors is virtually abolished. The gonadal mesoderm and fat body defects seen in zfh175.26; eyacli-IID double mutant embryos are identical to that seen in zfh165.34/zfh175.26 single mutant embryos.
zfh15/zfh175.26 is partially rescued by Scer\GAL4elav-C155/zfh1UAS.cLa
zfh15/zfh175.26 is not rescued by Scer\GAL4s.gcm/zfh1UAS.cLa
zfh15/zfh175.26 embryos expressing zfh1Scer\UAS.cLa under the control of Scer\GAL4elav-C155 show a substantial rescue in the ability of the ISNb and SNa nerves to exit the CNS, but does not rescue the ISN projection defects.
Germ cell migration phenotype is rescued by heat induced ectopic expression of zfh1hs.PL.