sdt^XP homozygous embryos exhibit defects in adherens junctions and apical polarity of epithelial cells.

sdt^XP mutant clones in genetically mosaic eye discs do not show a growth advantage compared to wild-type clones.

Embryos hemizygous for sdt^XP show severely reduced cuticle production, typically resulting in embryos with fragmented cuticle.

Homozygous eye clones results in bulky and irregularly shaped rhabdomeres. When exposed to light for 5 days, nearly all mutant photoreceptor cells survive.

Homozygous clones can cover large areas of the wing without any overt phenotype when abutting the dorsoventral boundary or when running along the longitudinal veins.

sdt^XP somatic clones in the early pupal eye (38% pupal development), zonula adherens structure is only mildly disrupted. These defects are no longer detectable by late pupal stages, or in the adult eye. Stalk membranes in adult sdt^XP mutant photoreceptors are reduced by 40% compared with the wild type, and are often smoother without the deep folds seen in wild-type. sdt^XP mutant rhabdomeres become irregularly shaped, frequently expanded, split, or in contact with neighboring rhabdomeres. The base membrane of microvilli in these rhabdomeres is severely disrupted by vesicle-like membrane structures concentrating around the base of the rhabdomere.

Marker analysis of photoreceptor cells in somatic clones of sdt^XP in pupal eyes (40-50% pupal development) indicates displacement/expansion of the adherens junction and associated F-actin baso-laterally from the apical position it occupies in wild-type. The apical domains of these photoreceptors fail to orient to the center of ommatidia, resulting in the formation of rhabdomeres in displaced positions. Rhabdomeres in these clones are also often fragmented: longitudinal sections reveal discontinuous, disrupted rhabdomeres. The most severe disruption/loss of rhabdomeres is seen proximally, whereas distally rhabdomeres are relatively well organised. In the distal region of adult eyes rhabdomeres in somatic clones of sdt^XP mutant cells are bulky and fused.

In sdt^XP germline clone embryos, an irregular cell shape and multilayered epithelial structure is seen at stages 11 to 12.

Homozygous embryos derived from germ line clones exhibit severe malformations or an absence of epidermis. They also exhibit abnormal zonula adherens formation and mislocalisation of membrane protein neurotactin.

sdt^XP has abnormal cell polarity | embryonic stage phenotype, suppressible by shg^ASSA.GFP/shg^ASSA.GFP

sdt^XP has abnormal cell polarity | embryonic stage phenotype, suppressible by shg^{S4A.α-Cat.GFP}/shg^{S4A.α-Cat.GFP}

sdt^XP has epithelial cell | embryonic stage phenotype, suppressible by shg^ASSA.GFP/shg^ASSA.GFP

sdt^XP has epithelial cell | embryonic stage phenotype, suppressible by shg^{S4A.α-Cat.GFP}/shg^{S4A.α-Cat.GFP}

sdt^XP has adherens junction | embryonic stage phenotype, suppressible by shg^ASSA.GFP/shg^ASSA.GFP

sdt^XP has adherens junction | embryonic stage phenotype, suppressible by shg^{S4A.α-Cat.GFP}/shg^{S4A.α-Cat.GFP}