Expression of ss cDNA sscA5 is governed by UAS regulatory sequences.
dendrite & dorsal multidendritic neuron ddaC, with Scer\GAL4ppk.PG
dendrite & tracheal innervating neuron, with Scer\GAL4477
leg | distal, with Scer\GAL4ptc-559.1
Expression of ssScer\UAS.A5 under the control of Scer\GAL4477 causes ectopic dendritic branches to form in the td neuron (the td neuron normally extends bipolar dendrites ventrally and dorsally with little or no branching).
Expression of ssScer\UAS.A5 under the control of Scer\GAL4ppk.PG causes a severe reduction in terminal branching of the dendrites in the ddaC neuron.
ssScer\UAS.A5; Scer\GAL4GMR.PF have normal retinal morphology but marker analysis indicates, transformation of pale ommatidium type R7 cells to a yellow-type ommatidium R7 cell fate and an abnormal rhodopsin expression profile in other eye photoreceptor subtypes. Apart from this, specification of inner vs outer photorecptor types and R7 vs R8 appears normal.
ssScer\UAS.A5; Scer\GAL4hs.PB animals given a 30 minute heat shock at mid-pupal stages have a range of eye phenotypes from ransformation of pale ommatidium type R7 cells to a yellow-type ommatidium R7 cell fate to an abnormal rhodopsin expression profile in other all eye photoreceptor subtypes. Heat shocks during larval or early pupal stage are lethal.
ssScer\UAS.A5; Scer\GAL4Pan-R7 have normal retinal morphology but marker analysis indicates, transformation of pale ommatidium type R7 cells to a yellow-type ommatidium R7 cell fate. This effect is also seen if the eyes are also homozygous for ssD115.7. In neither case is this phenotype accompanied by a shift of R8 cell fate from pale-type to yellow-type in the affected ommatidia.
ssScer\UAS.A5; Scer\GAL4GMR.long flies have rough eyes and an abnormal rhodopsin expression profile is seen in all eye photoreceptor subtypes.
When :ssScer\UAS.A5 is driven by Scer\GAL4sd-SG29.1, none of the adult mutant flies develop wings. When :ssScer\UAS.A5 is driven by Scer\GAL4sd-NP7148, adult mutant flies develop wings that show incisions into their wing margins. Overexpression of ssScer\UAS.A5 in clones in the wing (driven by Scer\GAL4Act5C.PI) leads to apoptosis in which cell autonomy is position dependent. Clones have a rounded shape.
When expression is driven by Scer\GAL469B, embryonic trachea and midline are disorganised. Expression driven by Scer\GAL4ptc-559.1 causes transformation of maxillary palp, rostral membrane and distal leg to antenna. Palps are also often deleted, as are medial leg structures. Anterior structures from the distal femur and most of the tibia are deleted. Much of posterior compartment remains, and produced irregular cuticular out growths. The distal basitarsus is retained and more distal tarsal segments are usually unaffected, with the exception of transformation of claw to arista. Central part of wing is deleted, a zone of polarity reversal occurs in the abdominal tergites and a few scattered bristles are induced in the wing.
Scer\GAL4NP7148, ssUAS.A5 has wing margin phenotype, suppressible by Dll5/Dll[+]
Scer\GAL4NP7148, ssUAS.A5 has wing margin phenotype, suppressible by tgoRNAi.UAS.cAa/Scer\GAL4NP7148
Diap1UAS.Tag:MYC, Scer\GAL4sd-SG29.1, ssUAS.A5 has wing phenotype
Diap1UAS.Tag:MYC, Scer\GAL4sd-SG29.1, ssUAS.A5 has pretarsus | ectopic phenotype
When thScer\UAS.T:Hsap\MYC and ssScer\UAS.A5 are co-expressed under the control of Scer\GAL4sd-SG29.1, an ectopic tarsus-like structure is is generated in the wing. When ssScer\UAS.A5 expressing clones are made in the wing disc, they retain a rounded shape, even after the addition of W05014 or hepCA.
ssUAS.A5/Scer\GAL4221 rescues ssD115.7/ss134
The primary branch overgrowth and increased terminal branching seen in ss134/ssD115.7 class I dendrites is rescued by expression of ssScer\UAS.A5 under the control of Scer\GAL4221.