Expressed in a tight cluster of somatic gonadal precursor cells at the anterior of embryonic stage 17 male gonads. It is also expressed in the adult hub. It is not expressed in female gonads.
No defects in dendrite pruning of ddaC dorsal dendritic arborising neurons are seen in homozygous clones at 18 hours after puparium formation.
2o and 3o pigment cells in esgG66 clones of the eye form a cell lattice at ~36 hours APF as occurs in wild-type eyes. However, the cells in the clone fail to undergo the apical restriction that usually follows the lattice stage. Cells within the clone show no obvious defects in actin cytoskeleton or cellular morphology.
esgG66 clones in the adult eye show a dramatic loss of 2o and 3o pigment cells resulting in gaps between ommatidia.
Transplantation experiments in which prospective germ cells from homozygous esgG66 embryos are transplanted into agametic hosts show that esg is dispensible for gametogenesis in both the male and the female germline as fertile male and female host animals which have integrated homozygous esgG66 donor germ cells have been recovered.
The size of the primary branches of the tracheal system is largely unaffected in mutant embryos, even though segments of the dorsal trunk are disconnected.
Homozygous clones induced in the leg disc at the late second larval instar stage are sometimes associated with ectopic fold formation.
The dorsal branch fusion cells form discrete branches that never meet or join. These cells go on to form additional branches that resemble normal terminal branches in the larva. Lateral trunk fusion branches are completely missing leaving a gap in each segment of the lateral trunk.
Failure of tracheal fusion in embryos. Tip cells do not accumulate shg in their filopodia, which migrate in other directions and no fusion occurs. Cell motility is hyperactivated in tip cells of both thin and thick tracheal branches. esgG66 P{HS-esg.F} embryos heat shocked seven times exhibit restoration of shg expression and adhesion, the trachea completely fuse.
esgG66 has secondary pigment cell | somatic clone phenotype, non-enhanceable by sna1
esgG66 has tertiary pigment cell | somatic clone phenotype, non-enhanceable by sna1
esgG66 has secondary pigment cell | somatic clone phenotype, non-enhanceable by worRNAi.1701.UAS/worRNAi.842.UAS/sna1/Scer\GAL4Act5C.PP
esgG66 has tertiary pigment cell | somatic clone phenotype, non-enhanceable by worRNAi.1701.UAS/worRNAi.842.UAS/sna1/Scer\GAL4Act5C.PP
Scer\GAL4Act5C.PP, esgG66, sna1, worRNAi.1701.UAS, worRNAi.842.UAS has pigment cell | somatic clone phenotype
Scer\GAL4Act5C.PP, esgG66, sna1, worRNAi.1701.UAS, worRNAi.842.UAS has eye photoreceptor cell | ectopic | somatic clone phenotype
Scer\GAL4Act5C.PP, esgG66, sna1, worRNAi.1701.UAS, worRNAi.842.UAS has cone cell | ectopic | somatic clone phenotype
esgG66, sna1 has haltere disc phenotype
esgG66, shghs.PU has larval tracheal system phenotype
esgG66, sna1 clones that express both wordsRNA.842.Scer\UAS and wordsRNA.1701.Scer\UAS, under the control of Scer\GAL4Act5C.PP, in the eye show ectopic photoreceptor and cone cells and a significant reduction of the pigment rim.
esgG66, sna1 clones show the same loss of 2o and 3o pigment cells as esgG66 clones. This phenotype is not enhanced in esgG66, sna1 Scer\GAL4Act5C.PP>wordsRNA.842.Scer\UAS, wordsRNA.1701.Scer\UAS clones.
The wing disc is absent in esgG66, sna1 double mutants, and the apical constrictions do not occur in the wing primordium cells. The haltere discs are similarly affected, but leg discs are unaffected. There is no sign of cell death in the prospective wing disc of the double mutant embryo. The mutant phenotypes can be rescued by either snahs.PF or esghs.PF.
Excision of the P{enG} element can revert the mutant phenotype.