Wing and leg disc development is normal in mutants.
3.0 +/- 0.1 midline glia (MG) are seen per segment in stage 12/0 mutant embryos (wild-type embryos have 5.6 +/- 0.2 MG cells per segment at this stage). At stage 17 mutant embryos have 2.6 +/- 0.1 MG per segment compared to the wild type 3.0 +/- 0.1 MG per segment. Mutant embryos show early defects in commissure formation; the first commissural axons extend randomly across the midline at stage 12/0. At stage 17, the commissural tracts appear uniform and well separated, although they are thinner than normal. The longitudinal tracts are reduced between segments and thicker within segments in stage 17 mutant embryos. Interruptions and defasciculation are also seen in the longitudinal tracts. Occasionally, Fas2-positive axons project across the commissural tracts.
vn[+]/vnunspecified is an enhancer of visible | dominant phenotype of EgfrE1
vnunspecified has phenotype, enhanceable by Egfrt1/Egfrf11
rhounspecified, vnunspecified has wing vein phenotype, suppressible | partially by EgfrE3/EgfrE3
vn[+]/vnunspecified is an enhancer of eye phenotype of EgfrE1
vnunspecified/vnunspecified is an enhancer of phenotype of Egfrt1/Egfrf11
Bant\lefUAS.cGa, Scer\GAL4Bx-MS1096, vnunspecified has wing vein phenotype
spi1, vnunspecified has larval longitudinal connective phenotype
spi1, vnunspecified has larval ventral nerve cord commissure phenotype
spi1, vnunspecified has larval ventral nerve cord | ventral phenotype
spi1 ; vnunspecified double homozygotes have one dorsal midline cell per segment and a reduction in the number of ventral neurons. The effect on the dorsal midline cells appears to be additive, while the effect on the number of ventral neurons suggests a genetic interaction between spi and vn. Most spi1 ; vnunspecified double homozygotes show complete fusion of the commissures and complete loss of the longitudinal tracts. Some embryos lack both longitudinal and commissural connectives, with most axons remaining within one hemi-segment. vnunspecified homozygotes that are also heterozygous for spi1 have a single fused commissure and variably reduced longitudinal connectives.
Strongly dominantly enhances the EgfrE1 rough eye phenotype.
Egfrt1/Egfrf11 vnunspecified/vnunspecified double mutants have a superadditive phenotype. The lack of vein phenotype of rhounspecified vnunspecified flies is partially rescued by EgfrE3/EgfrE3.
Moderate expression of Zzzz\lefScer\UAS.cGa under the control of Scer\GAL4Bx-MS1096 in vnunspecified heterozygotes results in wing vein loss, while moderate Zzzz\lefScer\UAS.cGa expression (with Scer\GAL4Bx-MS1096) alone doesn't have this phenotype.
