chp protein is abnormallly distributed in chp mutants. In chp1, levels of protein are reduced along the axons in larvae and pupae. In chp2, little or no protein is detected in third instar larval eye disc, in pupa, or in adult retina.
In mosaic retinas, chp2 and Synd661T double homozygous photoreceptor cells during pupal stages the stalk-rhabdomere separation is severely and prominently disrupted (even before catacomb-like membrane architecture formation); in adults microvilli show no co-adherence instead spread across the entire apical membrane adult mosaic retina when compared to controls.
prom1/prom1; chp2/+ double mutant flies show suppression of the prom1/prom1 rhabdomeral phenotype. However, in prom1/prom1, eys1/+; chp2/+ flies the rhabdomeres are stuck together, so the mild prom1/prom1; chp2/+ phenotype is enhanced in prom1/prom1, eys1/+; chp2/+ flies.
In prom1/prom1; chp2/+ double mutant flies, the proportion of flies with one aberrant fused cluster of rhabdomeres per ommatidium is smaller than in prom1/prom1 single mutants. In the double mutant flies, some ommatidia show the wild-type pattern of 7 individual rhabdomeres, while most ommatidia show between 2 and 5 individual rhabdomeres, and a small proportion show one fused cluster of rhabdomeres. In prom1/prom1, eys1/+; chp2/+ triple mutant flies, the rescue of the prom1/prom1 phenotype is reduced compared to the prom1/prom1; chp2/+ flies, with most ommatidia in the triple mutants showing between 0 and 3 individual rhabdomeres and no ommatidia showing more than 3 individual rhabdomeres.