Mutation resulting in alterations in the pattern of transcripts produced (truncated transcripts are produced in pupae).
Homozygotes have a broader wing blade than normal and have ectopic veins emanating from the posterior crossvein, posterior to L5 and between L2 and L3. The positions of veins L2 and L5 are shifted from the central anterior-posterior boundary towards the margins compared to wild type.
nmoadk2/nmoDB24 flies have more cells per given area of the wing blade compared to controls, suggesting that the mutant cells are slightly smaller than wild-type cells. In addition, the wings are consistently larger than wild-type wings.
Post death stage homozygous nmoadk2 pupal retinae have an increased average density of secondary/tertiary pigment cells compared to wild-type. Unlike wild-type, the local density of these cells is variable: dependent on the specific abberations in ommatidial shape and orientation in the region in question. In some regions the ommatidia are square-like and have approximately wild-type numbers of secondary/tertiary cells. In other regions of the same retina, ommatidia retain a hexagonal-like shape but have increased numbers of secondary/tertiary pigment cells. nmoadk2 pupal retinae have a decreased level of cell death compared to wild-type at multiple developmental time points.
nmoP1/nmoadk2 flies have a smaller eye than normal in which the ommatidia are square instead of the normal hexagonal shape and are generally flanked by 4 interommatidial bristles (instead of the usual 3 bristles at alternating corners). Mutant flies have a shorter, broader wing than normal. Excess wing vein tissue originating from the posterior crossvein and extending distally between veins L4 and L5 is seen (this phenotype is fully penetrant). Additional vein material can also form parallel to vein L2 and posterior to vein L5. The wings are held away from the body at a 45o angle. Polarity defects are seen in those regions in the wing where ectopic veins are seen. Homozygotes show a mild loss of bristles on the head and notum (having an average of 37.0 +/- 1.60 bristles compared to the wild-type number of 40) and occasionally have bent or duplicated bristles.
Semi-lethal, rare homozygous flies display rough, small eyes and several wing phenotypes. Wings are rounder and shorter and held out at an angle from the body, and also display ectopic cross vein material.
nmoadk2/nmoadk1 has visible phenotype, suppressible by Scer\GAL432B/E(spl)mβ-HLHUAS.cdCa
nmoadk2/nmo[+] is a suppressor of visible phenotype of Hsap\ATXN182Q.UAS, Scer\GAL4GMR.PU
nmoadk2/nmo[+] is a suppressor of abnormal eye color phenotype of Hsap\ATXN182Q.UAS, Scer\GAL4GMR.PU
nmoadk2/nmoadk1 has wing vein | ectopic phenotype, suppressible by Scer\GAL432B/E(spl)mβ-HLHUAS.cdCa
Df(2L)flp147E/+, nmoadk2 has wing phenotype
Heterozygosity for nmoadk2 partially suppresses the small eye size of rprGMR.PH animals. Wings from flies homozygous for nmoadk2 and heterozygous for Df(2L)flp147E are fragile and display apparent defects in epithelial integrity not normally observed in nmoadk2 mutants.
The mild wing vein thickening phenotype seen in Dl9M/+ flies is synergistically enhanced by homozygosity for nmoadk2. The ectopic wing veins seen in nmoadk2 flies are completely suppressed by H1. The loss of bristles on the head and notum seen in H1/+ flies is dramatically enhanced by nmoadk1/nmoadk2. Expression of HLHmβScer\UAS.cdCa under the control of Scer\GAL432B completely suppresses the extra wing vein phenotype of nmoadk1/nmoadk2 flies. px1 nmoadk2 double mutant flies show a synergistic interaction with respect to the extra wing vein phenotype of each single mutant. net1 nmoadk2 double mutant flies show a strong synergistic interaction with respect to the extra wing vein phenotype of each single mutant. dpps1 nmoadk2 flies show an enhancement of the nmoadk2 ectopic wing vein phenotype, especially in the anterior of the wing blade near vein L2.
Second site dominant suppressor of Nnucl.sev that reduces the external roughness of the eye, in addition to causing the overall eye shape to become both rounder and larger, and less refractile.
One copy of nmoadk2 strongly suppresses the retinal depigmentation and ommatidial disorganisation phenotype seen when Hsap\ATXN182Q.Scer\UAS is expressed in the eye under the control of Scer\GAL4GMR.PU.
nmoadk2/nmoadk1 is rescued by nmoc5-1.UAS/Scer\GAL4bs-1348
Expression of nmoc5-1.Scer\UAS under the control of Scer\GAL4bs-1348 rescues the extra wing vein phenotype seen in nmoadk1/nmoadk2 flies.