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.
Rho1V14.sev has visible phenotype, enhanceable by rin[+]/rinunspecified
Rho1V14.sev has eye phenotype, enhanceable by rin[+]/rinunspecified
Rho1V14.sev has phenotype, non-enhanceable by exe1
Rho1V14.sev has phenotype, non-suppressible by exe1
Rho1V14.sev is a non-enhancer of phenotype of exe1
Rho1V14.sev is a suppressor of phenotype of dsh1
Rho1V14.sev is a non-suppressor of phenotype of exe1
Partially rescues the ommatidial polarity phenotype of dsh1 mutants.
U. Weber