Vangstbm-6 testes have slightly (but significantly) fewer waste bags and normal individualization complexes (ICs) while they have a similar number of abnormal ICs when compared to controls.
Homozygous larvae show increased crossing of dendrites in the dendritic arbor of the ddaC class IV neurons compared to wild type.
The angle and direction of rotation of ommatidia is randomised in mutant eyes.
The directional preferences of growing microtubules in mutant wing cells is not significantly different from that seen in wild type at 24 hours after puparium formation.
In wild-type wings, the ratio of non-hexagonally shaped cells relative to hexagonally shaped cells is around 11%, whereas in Vangstbm-6 homozygous mutant wings this ratio increases to 30%.
Vangstbm-6 mutant wings display strong hair orientation defects, but very few if any multiple hairs.
Overall length of the tracheal dorsal trunk is normal in hemizygous stage 16 embryos.
Vangstbm-6 mutant border cells are predominantly found at the lagging edge of border cell clusters compared to wild-type cells that show a strong preference to migrate at the leading edge of the cluster.
Border cell clusters from Vangstbm-6 mutants show an average of 37 actin protrusions, reduced compared to the average of 94.8 in wild-type clusters.
In border cell clusters where both polar follicle cells are mutant for fz15 there is no preference for non-mutant border cells to take up the leading edge positions in the cluster, which is observed when polar cells are wild-type. In border cell clusters where only one polar follicle cell is mutant for fz15, this mutant cell displays no preference for position at the front or back of the cluster.
Homozygotes show defects in ommatidial polarity.
Vangstbm-6/VangA3 adults show defects in ommatidial patterning, with ommatidia pointing in random directions with randomised chirality.
Homozygous clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone.
The hexagonal packing of intervein cells, which usually occurs between wing development stage P2B (when the first morphological signs of veins appear (FBrf0005070), and the middle of P2C (before hair formation (FBrf0005070)) is disrupted in Vangstbm-6/Vangstbm-6 flies.
In Vangstbm-6 mutant pupae, the mitotic spindles of dividing sensory organ precursor cells in the developing notum are not aligned with the anterior-posterior axis, but instead are randomly oriented.
Vangstbm-6 flies are viable with a planar polarity phenotype in the tergites which resembles that seen in fz- flies: they are disheveled, especially in the anterior parts of the anterior compartment, but have largely normal polarity elsewhere. Similarly, in the pleura, polarity is generally disordered, as in fz-, except that there is a weak tendency for the hairs to be organized into zones of alternating polarity along the antero-posterior axis. The hairs in the middle of the anterior compartment tend to be reversed, with the remaining hairs being more normally polarised.
Within Vangstbm-6 somatic clones in the adult abdomen the rows of hairs are jumbled and poorly oriented: some hairs point straight upwards, especially those in clones in anterior regions of the anterior compartment. Disruption of polarity extends a few cells anterior to these clones. This non-autonomous effect is variable, usually including patches with some hairs that are reversed. Reversal anterior to clones is more consistent and extensive for clones in the pleura, but is unaffected by position on the anteroposterior axis and can extend across the A-P compartment boundary.
Vangstbm-6 homozygous embryos fail to hatch, exhibiting a phenotype similar to unfertilized eggs.
Mutants show no significant disruption of ovarian morphology.
Homozygotes are viable, although many embryos die between 0-4 hours after egg laying. Homozygotes have rough eyes, due to misalignment of the normally parallel rows of ommatidia. The majority of ommatidia in the eye are correctly assembled, and the misaligned eye lattice is due to aberrant orientation of ommatidial units, which can be in several orientations: normal (46%), reversed dorsoventrally (35%), reversed anteroposteriorly (7%) or reversed both dorsoventrally and anteroposteriorly (7%). In addition, although most ommatidia rotate the normal 90o, some undergo partial or no rotation (3%). Photoreceptors R3 and R4 are bilaterally symmetrical in 2% of ommatidia, abolishing the chirality of these ommatidia. These ommatidia show a rectangular rather than the normal trapezoidal arrangement of rhabdomeres. The pigment cell lattice is also disrupted, as a consequence of ommatidial misorientation. The eyes contain a normal complement of primary pigment cells, bristles and cone cells, although a few ommatidia are missing one cone cell. The number of secondary and tertiary pigment cells is often correct, except at the vertices of partially or unrotated ommatidia, where there is an excess of these cell types. Ommatidial assembly is normal in homozygous eye discs, but rotation of the ommatidia is delayed, and some ommatidia initiate rotation in the wrong direction. The polarity of many thoracic bristles is abnormal in homozygous adults, and the leg bristles are oriented perpendicular to the leg. Hair polarity is disrupted throughout the body, for example surrounding the eye and on the wings and thorax. Extra tarsal segments or partial duplications are frequently seen in tarsal segments 3 and 4, and occasionally in tarsal segment 2. The wings are held out.
In mutant eyes some ommatidia show normal polarity, many show inversions on the anterior-posterior and dorsal ventral axis so consequently the equator is abolished.