P{A92} insertion is located 28 nucleotides upstream of the 5' end of the cDNA.
ovary | adult stage (with RpS2PRW1)
RpS2P/RpS2P mutants are viable and cause female sterility. RpS2P/RpS2P and RpS2P/RpS2PRW1 ovaries exhibit a "string of pearls" phenotype wherein all egg chambers arrest development at stages two or three, and also exhibit abnormalities in germline stem cell divisions, abnormal spectrosomes, and delayed egg chamber growth.
Semi-lethal. The survival rate of sopP homozygotes is 10-15% of normal. Homozygotes eclose at least 2 days later than their wild type sibs. Egg chambers in homozygous mutant ovaries appear to develop normally until approximately stage 5, but development does not continue beyond this point. Homozygotes also show a mutant bristle phenotype. Macrochaetae on the thorax and head are shorter and thinner and more brittle than those of heterozygous siblings or wild type flies.
Homozygous females arrest oogenesis at stage 5. Bristle phenotype in males and females.
RpS2P/RpS2PRW1 has ovary | adult stage phenotype, enhanceable by Zfrp8[+]/Zfrp8SM206
RpS2[+]/RpS2P is an enhancer of ovary | adult stage phenotype of Scer\GAL4nanos.PU, Zfrp8GL00541
Zfrp8SM206/+ enhances the ovary phenotypes of RpS2P/RpS2PRW1 mutants.
RpS2P/+ enhances the ovary defects of flies expressing Zfrp8GL00541 under the control of Scer\GAL4nos.PU.
Δ2-3 revertants have lost the P{A92} insertion.