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.
sgg32 mitotic clones result in extra macrochaetae and microchaetae in the dorsal part and scutellum of the adult notum, which corresponds to the wg-expressing region.
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 sgg32 or sgg32/sggM11 adults (that have been rescued to adulthood by the addition of sgghs.P coupled with larval and pupal heatshocks), show a lengthening of the locomotor activity rhythm periodicity to about 26 hours.
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.
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.