abnormal locomotor rhythm (with sggM11), with sgghs.P
adult cuticle & abdomen | somatic clone
adult thorax & macrochaeta | somatic clone
adult thorax & microchaeta | somatic clone
macrochaeta & mesothoracic tergum | somatic clone | cell autonomous
macrochaeta & prescutum | somatic clone | cell autonomous
macrochaeta & scutum | somatic clone | cell autonomous
macrochaeta & wing | ectopic | somatic clone
29.2% of eggs derived from mothers carrying sgg32 mutant germline clones are able to complete meiosis. The remaining 70.8% exhibit abnormal meiotic defects.
Homozygous mutant clones give rise to ectopic bristles on the adult wing.
Homozygous clones in the anterior of the wing form small outgrowths.
sgg32 somatic clones in tergites are abnormally round in shape and have higher than normal bristle densities. In addition polarity reversals are seen; hairs and bristles at the back of clones are reversed. sgg32 somatic clones in the adult abdomen can transform segmental region anterior 1 (a1) cuticle into segmental region anterior 3 (a3) cuticle. Such clones in the segmental region posterior 2 (p2) can sometimes become hairy, suggesting a transformation to region p3.
Large homozygous clones that cover most of the dorsal wing hinge cause duplication of axillary sclerite 3 at the expense of axillary sclerite 1, axillary sclerite 2 and the unnamed plate. Clones in the ventral wing hinge cause reduction or loss of the axillary pouch, depending on the size of the clone.
Homozygous clones autonomously form extra macrochaetae in the notum. These appear most frequently near the dorsocentral meridian and in the scutellum and less frequently near the lateral macrochaetae. Extra macrochaetae are also seen medially in the scutum and prescutum, far from the normal site of any wild-type macrochaetae. The macrochaetae are confined to the posterior region of the clone, irrespective of the location of the clone in the notum.
sgg32 Df(1)sc-B57 clones in the wing show no disturbance in planar polarity.
Homozygous clones in the eye cause replacement of ommatidia by ectopic cuticle, which shows the typical ridged morphology of frons cuticle.
sgg32 mutant cells within clones present in the eye fail to differentiate and progression of the morphogenetic furrow is blocked. Wild type cells anterior to the clone fail to express neuronal markers confirming that the morphogenetic furrow is unable to reinitiate beyond a block caused by the wg pathway.
Clones of mutant cells induced in the leg show that removal of sgg activity is sufficient to specify ventral cell fate. Such clones can reorganise the dorsal-ventral axis of the leg. Ventrally located sgg clones show a local increase in bristle density due to a failure in lateral inhibition of neuronal fate specification. Bifurcations produced by clones in the tibia or femur are unable to extend beyond the end of the dsegment in which the bifurcation occurred. Dorsally located clones lead to the formation of duplicated legs by respecifying the fates of surrounding cells. Clones in lateral positions cause simple outgrowths of leg that consist entirely of mutant cells. The mutant cells do not affect the fate of the wild type cells around them. Mutant clones in the lateral region of the leg do not respecify cell fate. Pattern respecification occurs only when the clones are located dorsally, near the endogenous anterior-posterior compartment boundary. Duplicated legs always bifurcate from the dorsal side of the endogenous leg.
Homozygous clones in the thorax differentiate a cluster of bristles at the site of a single bristle in wild-type flies. In 98% of cases that respond, individual bristles of the same mutant cluster behave similarly to one another and elicit a cleaning response from the same leg. The mutant bristles elicit the same behavioural response as wild-type bristles when stimulated.
sgg32 has visible | recessive | somatic clone phenotype, enhanceable by Su(fu)LP
sgg[+]/sgg32 is a non-enhancer of abnormal locomotor rhythm phenotype of timblind
sgg32 is a suppressor of visible | recessive | somatic clone phenotype of NMcd1
sgg[+]/sgg32 is a non-suppressor of abnormal locomotor rhythm phenotype of timblind
sgg32 has wing | anterior | somatic clone phenotype, enhanceable by Su(fu)LP
sgg32 has wing phenotype, non-enhanceable by Atg4bP0997/Atg4bP0997
sgg32 has wing phenotype, non-suppressible by Atg4bP0997/Atg4bP0997
sgg32 has phenotype, non-suppressible by Rnor\Gsk3ahs.PR
sgg32 is an enhancer of macrochaeta | increased number phenotype of DroncC318G.UAS, Scer\GAL4sca-P309
sgg32 is an enhancer of wing margin bristle | ectopic phenotype of Scer\GAL4en-e16E, armUAS.cWa
The sgg32 mutation leads to an enhancement in the number of flies that show extra macrochaetae on the scutellum when NcC318G.Scer\UAS is expressed under the control of Scer\GAL4sca-P309.
Unlike Pka-C1E95 clones, sgg32 Pka-C1E95 double mutant clones in the medial prescutum produce macrochaetae autonomously, and unlike sgg32 clones, the double mutant clones have a symmetrical bristle pattern. Formation of macrochaetae within the double mutant clones is increased relative to sgg32 clones. In the posterior scutum, sgg32 Pka-C1E95 double mutant clones have a scutellar phenotype very similar to that of Pka-C1E95 clones. In the anterior scutum, sgg32 Pka-C1E95 double mutant clones no longer show the non-autonomous induction of macrochaetae or formation of pits characteristic of Pka-C1E95 clones. Formation of macrochaetae within the double mutant clones is increased relative to sgg32 clones.
No significant effect on the scaMSKF mutant phenotype.
Rnor\Gsk-3αhs.PR and Rnor\Gsk-3βhs.PR do not rescue sgg32 at all, even under maximal heat shock. Rnor\Gsk-3βhs.PR can rescue sgg32 in wing disc clones, therefore can replace sgg during the epidermal-neural cell fate decision, but not at other stages of life cycle that sgg is required.
sgg32 is rescued by sggUASp.cTa
Expression of sggScer\UAS.P\T.cTa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 rescues the meiotic defects seen in sgg32 mutant germline clones.
Ripoll.
None of the multiple products of the sgg locus remain in this allele.