adult thorax & microchaeta
axon & dorsal cluster neuron
leg & joint
mesothoracic tergum & trichome
Double-heterozygous flies of the genotype dsh/+ together with either kmr1/+ or kmr2/+ display misoriented hair patterns on the wing, thorax and eyes, while single heterozygotes exhibit phenotypes similar to wild-type controls.
Presence of FrlEx83/+ or FrlExK62/+ does not significantly alter eye phenotypes seen in dsh1/Y flies. Presence of dsh1/Y (or dsh1/+ females) does not significantly alter eye phenotypes in FrlEx83/FrlEx83 or FrlExK62/FrlExK62 clones. Presence of FrlEx83/+ or FrlEx88/+ does not enhance mushroom body axon growth defects seen in dsh1/Y flies.
One copy of dsh1 enhances the axonal projection defects seen in the α and β lobes of DAAMEx1 mutant mushroom bodies in females. Very few, if any, defects are seen in dsh1 DAAMEx1 double heterozygotes. DAAMEx1 enhances the axon projection phenotypes seen in dsh1/Y males alone. Many of these double hemizygous males exhibit an early growth termination phenotype not seen in either mutant alone.
Expression of dxΔNBS.Scer\UAS under the control of Scer\GAL4ap-md544 in a dsh1 background partially inhibits normal joint formation (this phenotype seen in dxΔNBS.Scer\UAS, Scer\GAL4ap-md544 single mutant) and partially suppresses the formation of ectopic leg joints seen in dsh1 single mutants.
Clones expressing fzScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Act5C.PI in a dsh1 background result in non-clonal cells pointing their trichomes away from the clone. This effect extends at most 3-4 cells from the clone boundary.
Expression of Rac1N17.Scer\UAS, under the control of Scer\GAL4ato.3.6, in a dsh1 background results in a dorsal neuron cluster phenotype similar to when Rac1N17.Scer\UAS is expressed in a wild-type background, which is opposite to that seen in dsh1 mutants.
Expression of hepScer\UAS.cBa, under the control of Scer\GAL4ato.3.6, in a dsh1 background results in a large increase of dorsal cluster neuron axons crossing the optic chiasm, indicating a complete dominance of the hep gain of function phenotype.
Expression of one copy of bskDN.Scer\UAS, under the control of Scer\GAL4ato.3.6, in dsh1 mutant animals results in a synergistic reduction of extension of dorsal cluster neuron axons, with 60% showing no axons crossing the optic chiasm.
Expression of btlDN.Scer\UAS under the control of Scer\GAL4ato.3.6 in a dsh1/+ background suppresses the reduction of dorsal cluster neuron axon extension phenotype seen in either single mutant, with the number of dorsal cluster neuron axons crossing the optic chiasm restored to almost wild-type levels.
The average number of cells having multiple wing hairs in a defined region of the wing (the ventral surface of the proximal-anterior region) is reduced by more than 7-fold in dsh1 males that are also expressing rokαTub84B.PW compared to dsh1 single mutants. The hair misorientation phenotype is not suppressed. Suppression of ectopic F-actin-rich prehairs is seen in double mutant pupae, but the abnormal assembly of the prehair at the centre of the cell is not suppressed. Addition of rok2 to dsh1 mutants results in a 2.5-fold increase in the number of multiple wing hair cells compared to dsh1 single mutants. The dsh1 multiple hair phenotype but not the hair misorientation phenotype is suppressed by sqhE20.E21.
Double mutants of VangTbs42, VangA3 or VangA5 with fz24, dsh1 inunspecified and mwhunspecified all showed hair polarity pattern typical of the fz-in group. Multiple hair cell phenotypes of the cell autonomous dsh, in and mwh mutants are epistatic to Vang. Show no interaction with the dominant wing basal cell 1 swirl phenotype of VangTbs42.