fusion competent cell & visceral mesoderm
muscle founder cell & visceral mesoderm
Heterozygous DlB2 mutants display thickened veins and deltas at the margin of adult wings.
DlB2/+ adult flies display thickened veins ending in deltas.
DlB2/+ flies have a wild-type number of scutellar macrochaetae.
Marker expression and morphology suggest that numbers muscle founder cells are increased at the expense of fusion competent myoblasts in the visceral mesoderm of stage 11 DlB2 mutant embryos.
Mutant embryos are extremely deformed are do not always have a recognisable hindgut.
Heterozygotes with SerBd-3 are viable and exhibit a severe wing phenotype.
DeltaB2 has visible | adult stage phenotype, suppressible by HattP/H[+]
DeltaB2 has visible | adult stage phenotype, suppressible by H[+]/HΔM3
DeltaB2 has visible | adult stage phenotype, suppressible by HΔM1-2/H[+]
DeltaB2 has visible | adult stage phenotype, suppressible by H[+]/HCfs
DeltaB2 has visible | adult stage phenotype, non-suppressible by Hcwt/H[+]
DeltaB2 has visible | adult stage phenotype, non-suppressible by HΔM1/H[+]
DeltaB2 has visible | adult stage phenotype, non-suppressible by HΔM2/H[+]
Dl[+]/DeltaB2 is an enhancer of visible phenotype of Scer\GAL4lz-gal4, sensUAS.cNa
DeltaB2 is an enhancer of visible phenotype of Myt1GMR.PP
DeltaB2 has wing vein | adult stage phenotype, enhanceable by CycGHR7/CycGHR7
DeltaB2 is an enhancer of eye phenotype of Myt1GMR.PP
The vein thickening and vein deltas characteristic for HattP/+ adults is partially suppressible by combination with a single copy of HattP and to a lesser extent also by heterozygosity of HΔM3, HΔM1-2 or HCfs but no significant rescue is observed upon combination with one copy of Hcwt, HΔM1 or HΔM2.
DlB2/+ cannot restore the formation of interommatidial bristles in Df(1)sc10-1/Y flies.
Expression of sensScer\UAS.cNa under the control of Scer\GAL4lz-gal4 can restore the formation of interommatidial bristles in Df(1)sc10-1/Y flies. If the flies also carry DlB2/+, the number of bristles formed is further increased and there is a further loss of the normal ommatidial surface architecture.