Ommatidial rotation is severely disrupted in Rho1V14.sev mutants. 40.8% of ommatidia in mutant somatic clones in the eye are normal. 3.3% have rotated ommatidia, none have chirality defects, none are achiral (55.9% unscorable).
Low levels of expression of Rho1V14.sev leads to photoreceptor loss but no significant polarity defects. At higher levels polarity defects become apparent. Misorientated clusters are present from the earliest detectable stage and are thus primary defects.