Most hhbar3/hhbar3 mutant adults exhibit a small reduction in the area between wing veins L3 and L4, and a small minority exhibit wing blisters, as compared to controls.
hh2/hhbar3 mutant adults exhibit smaller wings with an ectopic crossvein, as compared to controls.
hhbar3 mutant eye diss exhibit ommatidial developmental defects.
The eyes of hh8/hhbar3 flies are smaller than wild-type and are slightly rough, due to some disorganisation of ommatidial and inter-ommatidial structure.
Homozygotes have a rough eye which has an indented anterior side.
hhbar3/hh8 flies have a slight rough eye phenotype.
hhbar3 heterozygotes are not significantly different from wild-type.
hhbar3 is a strong, eye-specific hypomorph. It is fully recessive in trans to wild-type, but has a severely reduced eye when homozygous (68% smaller than hhbar3/+) and in trans to the null hhAC it is smaller still (82% smaller than hhbar3/+). This suggests that hhbar3 is not an amorph for eye size by Muller's test: the phenotype becomes stronger in trans to the null.
hhbar3 homozygotes have about 10 columns of ommatidia compared to 28 to 30 in wild-type.
hhbar3/hhAC mutants exhibit about six columns of ommatidia per eye compared to 28-30 columns in wild-type.
R7 and R8 photoreceptor cell growth cones still form two layers in the medulla in hhbar3 animals, although they remain closely associated during the early pupal stage (17% APF).
dac-positive lamina neurons fail to differentiate in hhbar3 mutants.
The morphogenetic furrow becomes arrested in the eye discs of third instar mutant larvae.
The compound eyes of mutant animals lack anterior structures.
Flies homozygous for hhbar3 have narrow kidney-shaped eyes.
In hhbar3 mutant eye discs, most of the ommatidial clusters over-rotate, with 33.7% of them reaching 110o, compared to only 1.4% in wild-type discs (most ommatidial rotation in wild-type eye discs of late third larval and early pupal stages is about 50o-60o). The overrotation defect in these mutant discs correlated with the disappearance of the morphogenetic furrow (MF): In late third instar mutant eye discs the MF is still present, and most ommatidial clusters rotate to the normal position of 50o-60o, apart from a few in the most posterior region that over-rotate. As development progresses the MF becomes increasingly disrupted, and the over-rotation phenotype becomes more prominent. By the time MF progression is completely disrupted most of the ommatidial clusters have over-rotated, with many of them reaching 110o-120o. This overrotation phenotype persists to the adult stage, where 47.3% of ommatidia have a rotation degree larger than 105o, compared to 1.1% in wild-type.
In hhbar3 mutant larvae the posterior eye field develops normally, but anterior progression of the morphogenetic furrow is inhibited.
A small number of lamina neurons develop compared to wild type in hhbar3 animals. The development of glial cells is not affected. R1-R6 axons stop in the lamina (as in wild type) in these animals. The array of R7 and R8 growth cones in the medulla is indistinguishable from wild type.
Defective spatial positioning of the R7,8 axons is seen in 18% of hhbar3 homozygotes. Sometimes in just one lobe, and others in both. In the cases where both are affected the direction of the misorientation is the same.
Heterozygotes show a quantitative effect on wing shape in intervein regions C and D compared to wild type.
The eye is reduced in homozygotes, containing approximately 13 vertical rows of ommatidia from the posterior end.
Homozygotes have extremely reduced eyes, which contain approximately 150 (rather than the normal 800) ommatidia.
The eye discs contain about 11 columns of ommatidial R cell clusters. The most anterior clusters appear normal and the axon fascicles from them are found in their proper dorsoventral positions posterior to the lamina furrow. But viewed on their antero-posterior axis the fascicles are collapsed on each other. Glial cells are absent from the optic stalk and lamina. Lamina precursor cells fail to undergo their terminal division, arresting in G1 at the lamina furrow.
Homozygotes lack portions of the anterior eye, due to a defect in morphogenetic furrow progression. Eye phenotype is suppresses when in combination with Pka-C1DN heterozygote, cell death is also suppressed.
Arrests morphogenetic furrow movement after differentiation of 8-10 rows of photoreceptors. In wgl-12; hhbar3 eye discs the hhbar3 mutation completely abolishes the effects of loss of wg expression (inwardly directed furrow movement is not present).
An eye specific hh allele. Double mutants of bunrI043 and hhbar3 all die as pupae.
Adult eye is reduced in size. hhbar3/hh6 produces an intermediate reduced eye phenotype.
When in combination with Df(2R)enE/en1 a phenotype reminiscent of a weak dpp mutation is produced, narrowing of the space between wing veins 3 and 4. Posterior wing clones affect adjacent cells of the anterior compartment and cause an overall reduction in wing size.
The progression of the morphogenetic furrow in the developing eye disc arrests. The eye disc appears normal at the time of arrest. dpp expression is abolished (as assayed with a dpp-lacZ fusion gene).
Slight increase in bristles of all tarsal rows in the second leg.
Transheterozygotes with hhAC display an eye phenotype at 25oC.
A weak hypomorphic allele that is not complemented by other hh alleles. Eye of homozygote small and narrow with about 150 facets. Eye disc size reduced; deep cleft at anterior edge cell; clusters at cleft look mature (Renfranz and Benzer, 1989). viable