P{Mae-GMR.EP} inserted immediately upstream of the transcription start site of hbs.
microchaeta & adult thorax
hbsEP/hbsEP and hbsEP/Df(2R)δ12 pupal/pharate adult animals have a low incidence of fused ommatidia and wrong numbers of cone cells per ommatidium (<5% ommatidia) and a higher incidence of abnormal contacts between cone cells (50-60% ommatidia). These abnormal contacts reflect arrested cone cell morphogenesis: many cone cells maintain juvenile morphology and cell contacts in the adult. Adherens junctions between these cone cells appear normal, suggesting that this phenotype is not due to some general defect in junction formation or maintenance. These cone cell defects are also caused by somatic clones of hbsEP homozygous cells in the developing retina. The effect is autonomous to individual ommatidia: all ommatidia with defective cone cell contacts have at least one cone cell that is mutant.
hbsEP/hbsEP adults also have a low incidence of tissue polarity defects (<4% ommatidia) and occasional extra-interommatidial cells including extra interommatidial bristles. Thoracic microchaetae are also mis-patterned, leading to bald patches.