Premature stop codon in the N-terminal region.
Nucleotide substitution: C?T.
Amino acid replacement: Q76term.
C1860986T
Q76term | Rap1-PA; Q76term | Rap1-PB; Q76term | Rap1-PC
Q76term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
RrvB3 mutant eye clones show the frequent loss of R7 photoreceptors from the ommatidia, with less frequent loss of other photoreceptors and pigment cells.
RrvB3 mutant eye clones induced early in larval life result in large retinal scars, rich in pigment cells but almost completely lacking photoreceptors. Deeper sections of these preparations show a multitude of photoreceptors lying below the base of the retina, flattened above the outer nuclear layer of the lamina.
RrvB3 mosaic eye clones exhibit R2, R3, R4, R5 and R8 photoreceptors at high frequency, with many fewer R1/6 photoreceptors and few very R7 photoreceptors.
RrvB3 mutant eye clones in a minute background display extensive ommatidial differentiation, with expression of photoreceptor and lens cone cell markers but the specific absence of R7 markers.
Wild type eyes. Transheterozygotes with Df(3L)R-E are late larval lethal.
R[+]/Rap1rvB3 is a suppressor of eye phenotype of sevAct.hs2sev
R[+]/Rap1rvB3 is a suppressor of photoreceptor cell R7 | increased number phenotype of sevAct.hs2sev
R[+]/Rap1rvB3 is a suppressor of ommatidium phenotype of sevAct.hs2sev
Removal of one copy of R (sevAct.hs2sev/+; RrvB3/+) results in a decrease the eye roughening and a significant reduction in the multiple R7 phenotype (from 90% of the ommatidia containing multiple R7 cells to 48%).
Mutation has no effect on the rough eye phenotype caused by two insertions of P{GMR-Rho1}.
Revertant.
Fail to produce mitotic clones in the eye, this is consistent with an essential role of R gene product in cell proliferation or cell viability.