Overexpression of hbsScer\UAS.cDa under the control of Scer\GAL4hs.2sev results in eye planar cell polarity (PCP) defects including chirality and ommatidial rotation defects and also some photoreceptor cell loss.
Overexpression of hbsScer\UAS.cDa in the posterior compartment of the wing under the control of Scer\GAL4en-e16E results in wing notching.
Clonal expression of a single copy of hbsScer\UAS.cDa within an inter-ommatidial cell (under the control of Scer\GAL4GMR.PF) leads to partial segregation of the hbs-expressing inter-ommatidial cell. Typically, the hbs-targeted inter-ommatidial cell retains contact with one ommatidium and is flattened against it but is segregated away from the second ommatidium by neighboring inter-ommatidial cells, suggesting reduced adhesion between the hbs-targeted inter-ommatidial cell and ommatidia. Interestingly, the neighboring inter-ommatidial cells are part of the larger inter-ommatidial cell hexagonal lattice, which establishes across the hbs-targeted inter-ommatidial cell as if it is part of the adjacent ommatidium. Neighboring inter-ommatidial cells establish abnormally large interfaces with the hbs-targeted inter-ommatidial cell, suggesting adhesion between the hbs-targeted inter-ommatidial cell and neighboring inter-ommatidial cells is stronger than adhesion normally observed between inter-ommatidial cells.
Primary pigment cell precursors in hbsScer\UAS.cDa; Scer\GAL4Act5C.PI somatic clones are expanded compared to adjacent wild-type primary pigment cell precursors. When these somatic clones are induced at 18 hours APF, the clones have a reduced apical profile and are excluded from the flow of the ommatidial lattice. When these somatic clones are induced at 3-6 hours APF, inter-ommatidial precursor cells (IPCs) within clones have an abnormally large border and straight with neighboring wild-type IPCs. These cells also form ectopic septate junctions.
When hbs is expressed ubiquitously using hbsScer\UAS.cDa; Scer\GAL4hs.PB with heat shock at 25 hours APF, the polarized pattern of cell junctions of inter-ommatidial precursor cells at 27 hours is disrupted.
When hbsScer\UAS.cDa is driven by Scer\GAL4elav.PLu, Scer\GAL4da.G32 or Scer\GAL4sca-537.4 no defects are seen in axon guidance, or in glial cell placement and number. When hbsScer\UAS.cDa is driven by Scer\GAL4twi.PG myoblast fusion is partly disrupted in all hemisegments, but muscle fibre number and sites of muscle attachment are not. When hbsScer\UAS.cDa is driven by Scer\GAL4da.G32 myoblast fusion is partly disrupted in all hemisegments. Some muscle fibres are also inserted at inappropriate attachment locations. When hbsScer\UAS.cDa is driven by Scer\GAL4en-e16E disrupts attachments made by several lateral muscle fibres in most hemi-segments of all embryos. When driven by Scer\GAL4sca-537.4 disrupted attachments are seen in all hemisegments of all embryos. When driven by Scer\GAL4pnr-MD237 dorsal muscle attachments sites are radically disrupted, with the muscle fibres often failing to cross the segment and instead aligning with the segment boundary. Un-fused myoblasts are also seen in these combinations. When hbsScer\UAS.cDa is driven by Scer\GAL4da.G32 or Scer\GAL4bi-md653 an abnormal distal wing margin is seen. When driven by Scer\GAL4bi-md653 the distal wing edge is blistered, when driven by hbsScer\UAS.cDa it is blistered or notched. When hbsScer\UAS.cDa is driven by Scer\GAL4pnr-MD237, Scer\GAL4sca-537.4 or Scer\GAL4da.G32 the arrangement, but not the numbers of microchaetae on the central scutum is altered. When hbsScer\UAS.cDa is driven by Scer\GAL4GMR.PF or Scer\GAL4sca-537.4 a rough eye phenotype is seen - ommatidia and bristles are disorganised. When driven by Scer\GAL4da.G32, a strong rough eye phenotype is seen., with ommatidia occasionally fusing. Te photoreceptor clusters are irregularly placed in these adults and pigment cells are absent at sites of ommatidia fusion, though larval pathfinding and targeting in the developing eye appear normal.