When homozygous clones are induced in females using a technique that ensures that all eggs produced by these females are derived from homozygous germline clones and 76% of the follicles also carry homozygous somatic clones, then none of the cuticles of the resulting embryos have a dorsalised phenotype.
When homozygous clones are made in the follicle cells, no dorsalisation phenotypes are seen in the resulting embryos.
Migration of the mesoderm fails to occur properly in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic sgl function). The early steps in tracheal branching are significantly disturbed in stage 13 homozygous embryos (lacking zygotic sgl function). By late stage 15, tracheal branch formation is incomplete, as shown by the presence of large gaps in the dorsal and lateral trunks and stalled ganglionic branches. The penetrance of this phenotype is incomplete and the expressivity is variable; 7% of embryos show some degree of tracheal abnormality, ranging from one to all segments having breaks in the dorsal trunk. Virtually no tracheal branches are seen in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic sgl function).
Embryos derived from homozygous germ line clones in females have a cuticle phenotype identical to wg- embryos. This phenotype is zygotically (paternally) rescuable, but not to wild-type; zygotically rescued embryos have weak segmental fusions in the ventral part of the embryo and are often missing dorsal cuticle pattern elements. Homozygous clones in the wing result in the loss of anterior margin bristles and wing tissue.
Homozygous embryos derived from heterozygous females die at the third larval instar or early pupal stage. Homozygous embryos derived from females with homozygous sgl08310 germline clones die as embryos with a severe segment polarity phenotype. These embryos can be partially rescued by a paternal wild-type copy of sgl; 30% of paternally rescued embryos exhibit a weak segment polarity phenotype (partial fusion of the denticle bands) and do not hatch. Homozygous embryos derived from females with homozygous sgl08310 germline clones have 2-3 invaginations in the dorsal epithelium of the foregut (which will give rise to the stomatogastric nervous system) that are fused at the base. The second midgut constriction is not formed. The Malpighian tubules are very short.
Hemizygotes die between the first and second larval instar stages. Homozygous embryos derived from homozygous female germ-line clones show a loss of naked cuticle and a mirror-image duplication of denticle belts. This phenotype is fully rescued if the embryos receive a wild-type copy of sgl from their father. Homozygous somatic clones induced in second instar imaginal discs show no mutant phenotype in any part of the wing or other adult tissues.
Germline clones produce eggs with patterning defects: unrescued embryos exhibit mirror image duplication of denticle belts, rescued embryos are wild type or exhibit partial fusion of denticle belts.
sgl[+]/sgl08310 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702
sgl08310 has mesoderm phenotype, suppressible by Scer\GAL4twi.PG/htlλ.UAS
sgl08310 has larval tracheal system phenotype, suppressible by bnlUAS.cSa/Scer\GAL469B
sgl08310 has embryonic/first instar larval cuticle phenotype, suppressible by Scer\GAL4prd.RG1/wgl-12.UAS
sgl[+]/sgl08310 is an enhancer of larval posterior commissure | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702
sgl08310 is a suppressor | partially of larval tracheal system phenotype of Scer\GAL469B, bnlUAS.cSa
dallyΔP-188, sgl08310 has embryonic epidermis phenotype
The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly enhanced if the embryos are also heterozygous for sgl08310.
The mesoderm migration defects of sgl08310 embryos lacking both maternal and zygotic sgl function are partially rescued by htlScer\UAS.T:λ\cI-DD expressed under the control of Scer\GAL4twi.PG. Some tracheal branching is recovered if bnlScer\UAS.cSa is expressed under the control of Scer\GAL469B in sgl08310 embryos lacking both maternal and zygotic sgl function. The tracheal branching defects produced by expression of bnlScer\UAS.cSa under the control of Scer\GAL469B are weakly blocked if the embryos are homozygous for sgl08310.
Embryos heterozygous for dallyΔP-188 derived from mothers heterozygous for sgl08310 show cuticle defects characteristic of a reduction in wg signalling.
sgl08310 embryos expressing wgl-12.Scer\UAS under the control of Scer\GAL4prd.RG1 show a minor rescue of the sgl08310 cuticle phenotype, although naked cuticle is not specified.
Expression of wgl-12.Scer\UAS under the control of Scer\GAL4prd.RG1 in sgl08310 embryos does not generate naked cuticle. Expression of wgScer\UAS.cKa under the control of Scer\GAL4prd.RG1 in sgl08310 embryos induces naked cuticle at 25oC. Narrow regions of naked cuticle are produced when wgScer\UAS.cKa is expressed under the control of Scer\GAL4prd.RG1 in sgl08310 embryos at 16oC. Expression of hhScer\UAS.cIa under the control of Scer\GAL4prd.RG1 in sgl08310 embryos induces naked cuticle at 16oC and 25oC. Expression of armS10.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4prd.RG1 in sgl08310 embryos induces naked cuticle.
Dominantly enhances the weak phenotype of dsh4/Y flies carrying one copy of dshw, increasing the proportion of these flies that have defects in adult structures. sgl08310 homozygotes that are fully rescued by a single copy of sglUbi-p63E.PH die as second instar larvae if they are also heterozygous for wgen11.
sgl08310 is rescued by sglUbi-p63E.PH
Homozygotes are generally completely rescued by sglUbi-p63E.PH, although some sglUbi-p63E.PH lines show partial rescue, producing flies with distal deletions of wing veins.
A. Spradling.
Complements: sfl03844. Complements: argos05959. Complements: l(3)L4060L4060.
Somatic clonal analysis indicates that sgl acts non-cell-autonomously.