Imprecise excision of P{RS3}CB-0229-3 deletes 135 nucleotides, including the transcriptional start site and the first 18 codons of the protein. This deletion also disrupts the mitochondrial targeting sequence.
Approximately 90% of rho-7pΔ1 flies die before pupariation. Death occurs during both embryonic and larval stages, but those that survive to pupariation develop to adults, although approximately 10% of these die during the process of eclosion, and they get stuck while crawling from the pupal case. Surviving flies appear morphologically normal but all die within 3 days. Males are sterile but the females are fertile. The progeny of homozygous females exhibit exactly the same severity of phenotype as their parental generation and are not rescued by wild-type sperm, demonstrating that there is no maternal or paternal rescue of the homozygous zygotic phenotype.
The testes of homozygous rho-7pΔ1 males do not exhibit gross morphological disruptions, although the seminal vesicle is small and appears empty with no mature sperm.
rho-7pΔ1 mutant testicles exhibit irregularly-shaped nebenkerns, composed of many individual mitochondria that have coalesced beside the nucleus, but have failed to fuse.
Surviving adult rho-7pΔ1 mutants are morphologically normal, with the exception ofa wing-position defect, in which the wings of about 60% of individuals hang down on either side of the abdomen. The indirect flight muscles of these mutants exhibit a general disruption of the normal continuous pattern of the phase-dark banding. They exhibit numerous small mitochondria in the space between the myofibrils, as compared to larger mitochondria that completely fill the intramyofibril space in control flies.
rho-7pΔ1 mutant flies live for only 3 days. These flies also have extreme difficulty walking, and display erratic twitching in their legs and head. Synaptic transmission across the retina is impaired in rho-7pΔ1 flies. Both on- and off-transients are significantly smaller in rho-7pΔ1 flies compared to controls, with the off-transients exhibiting strong time and intensity dependency. The response of photoreceptors in rho-7pΔ1mutants is less than half of those of control photoreceptors, indicating reduced responsiveness to repetitive stimulation.
After 3 days of continuous light, rho-7pΔ1 mutant photoreceptors degenerate severely, with an almost complete loss of distinct rhabdomeres. These eyes show no detectable degeneration under normal light or dark conditions.
rho-7pΔ1 is a non-suppressor of visible | adult stage phenotype of Pink1UAS.Tag:HA, Scer\GAL4GMR.PF
rho-7pΔ1 is a suppressor | partially of wing phenotype of Scer\GAL4Bx-MS1096, fogUAS.cRa
rho-7pΔ1 is a suppressor | partially of wing | male limited phenotype of Scer\GAL4Bx-MS1096, fogUAS.cRa
rho-7pΔ1 is a non-suppressor of eye | adult stage phenotype of Pink1UAS.Tag:HA, Scer\GAL4GMR.PF
rho-7pΔ1 is a non-suppressor of ommatidium | adult stage phenotype of Pink1UAS.Tag:HA, Scer\GAL4GMR.PF
Approximately 43.5% of Scer\GAL4Bx-MS1096>fogScer\UAS.cRa/rho-7pΔ1 males show rescue of the wing phenotype whereas 37% show only a partial rescue, indicating that rho-7 is a suppressor of fog signalling.
rho-7pΔ1 does not suppress the disorganised eye phenotype seen when Pink1Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PF.