ommatidium | adult stage (with Vangstbm-6)
wing basal cell 1 & wing hair
VangA3 mutant clones non-autonomously reorient the wing hairs of neighbouring wild type cells so that they point away from the clone.
Vangstbm-6/VangA3 adults show defects in ommatidial patterning, with ommatidia pointing in random directions with randomised chirality.
48.0% of ommatidia in Df(2R)w45-30n/VangA3 mutant somatic clones in the eye are normal. 14.1% have rotated ommatidia, 36.8% have chirality defects, 0.9% are achiral (0.2% unscorable).
Shows a weak and incompletely penetrant dominant wing hair phenotype, as well as the reliable recessive phenotype wing hair tissue polarity phenotype. Phenotype falls between that of the fz-like and in-like classes of phenotype. Clonal analysis with VangA3 reveals that Vang acts cell nonautonomously, and shows domineering nonautonomy.
VangA3 has abnormal planar polarity | somatic clone phenotype, suppressible by fz23
VangA3 has abnormal planar polarity | somatic clone | cell non-autonomous phenotype, suppressible by pkD
VangA3 is a non-suppressor of abnormal planar polarity | somatic clone phenotype of fz23
VangA3, stan[+]/stanE59 has abnormal neuroanatomy | third instar larval stage phenotype
VangA3, pkD has abnormal planar polarity | somatic clone | cell non-autonomous phenotype
VangA3 has first basal wing cell phenotype, enhanceable by fz[+]/fz30
VangA3 has wing hair | somatic clone phenotype, suppressible by fz23
VangA3 has wing | somatic clone | cell non-autonomous phenotype, suppressible by pkD
VangA3 is a non-suppressor of wing hair | somatic clone phenotype of fz23
VangA3, stan[+]/stanE59 has dendrite | third instar larval stage phenotype
VangA3, stan[+]/stanE59 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
VangA3, pkD has wing | somatic clone | cell non-autonomous phenotype
Double mutants of VangTbs42, VangA3 or VangA5 with fz24, dsh1 inunspecified and mwhunspecified all showed hair polarity pattern typical of the fz-in group. Vang is epistatic to pk; double mutants of VangTbs42, VangA3 or VangA5 with pk1 show a fz-in group phenotype, possible less severe than for the Vang single mutant. VangA3 and VangTbs42, but not Vang11-3 act as dominant enhancers of the dominant phenotype of Df(2R)pk78s. VangA3 is a strong dominant enhancer of fz24. In double mutant combinations between VangA3, VangA5 and VangTbs42 with fz1, fz25 and fz30, the fz-in type of polarity pattern was slightly less abnormal than in either single mutant. The domineering nonautonomy of VangA3 clones can be suppressed by fz25 and fz30. VangA3 suppresses the domineering nonautonomy of fz23 clones.
Vangstbm-6/VangA3 is rescued by VangAct5C.EYFP
Vangstbm-6/VangA3 is partially rescued by VangUAS.cLa/Scer\GAL4GMR.PY
Vangstbm-6/VangA3 is partially rescued by Vangsev.PS
VangAct5C.T:Avic\GFP-EYFP can rescue the wing planar polarity defects seen in Vangstbm-6/VangA3 animals. Expression at 6 hours after puparium formation (APF) results in only minor polarity defects in the rescued wings. The rescue progressively worsens if expression is induced between 12 and 24 hours APF, with expression induced at 30 hours APF providing no rescue.
Vangsev.PS partially rescues the ommatidial patterning defects of Vangstbm-6/VangA3 adults. The ommatidial misrotation defect is largely rescued, but the dorsoventral inversion phenotype is not rescued.