Rearrangement in the genomic DNA approximately 5kb upstream from the first exon of the β transcript.
In nub2 mutants, the axonal projections to glomeruli VL2a, DL2d, VL2p, DP1I, VA7I, VM7c, VM7d, VM5v, VM2, VA2, DM5, VM5d, DA2, VA6, VA3, DM6, VA7m, VA1v, DA4m and DC3 are abolished while the projections to DL3, VA1d, and DL4 remain.
nub2 olfactory organ cell clones induced at 0 hours after puparium formation oly generate inner-cell clones.
Mutant flies lack the wing hinge.
Wings are smaller and shorter than normal and are abnormally folded and bent. Wing size reduction is due to reduced number of wing cells. Bristles of the triple row are incorrectly differentiated. Bracteated bristles can be seen in distal position, indicating a failure in proximo-distal specification. Wing vein L4 and crossveins are absent. Haltere is smaller than wild type. Third larval instar mutant wings exhibit conspicuous cell mortality. Clones in the wing are small and cause reduction of the whole wing size. Clones covering the proximal wing vein L2 causes thickening and those covering the triple row cause bracteated bristles.
Wing blade reduced, wing hinge is partially deleted. Wing margin is reproducibly interrupted at the tip of the wing. Clonal analysis reveals that mutant clones are considerably smaller than wild type clones, though the autonomous reduction in size is insufficient to explain the overall reduction in size of mutant wings. Clones which occupy a portion of the wing hinge cause a non-autonomous reduction in the size of the wing.
Wings small and spoonlike but less extreme than nub. Patches of dried blood on wings. Veins L1 to L4 almost indiscernible; L5 and alula frequently absent. Viability and fertility excellent. RK1.
R. F. Grell, 1st June 1956.
"X ray" was stated as tentative.