P{lacW} insertion in the middle of the 5' untranslated leader between nucleotides -15 and -16 relative to the translation initiation codon.
RpS131 heterozygous larvae show increased apoptosis in imaginal discs.
Heterozygous RpS131 mutant females exhibit a dilated cardiomyopathy phenotype, including an increased end-systolic dimension (EDD) and a decreased fractional shortening (FS) compared to controls. Bristles appear short and thin compared to wild type (Minute phenotype).
RpS131/+ flies have shorter and thinner scutellar bristles.
Minute phenotype.
RpS131/RpS13[+] is an enhancer of visible phenotype of Pi3K92ED954A.UAS.Tag:MYC, Scer\GAL4Bx-MS1096
RpS131/RpS13[+] is a suppressor of increased cell death | somatic clone | larval stage phenotype of Polr1Bk16513
RpS131/RpS13[+] is a non-suppressor of decreased cell number | somatic clone | larval stage phenotype of Polr1Bk16513
RpS131/RpS13[+] is an enhancer of wing phenotype of Pi3K92ED954A.UAS.Tag:MYC, Scer\GAL4Bx-MS1096
The proportion of embryos displaying a delay in furrow formation drops from 25% observed for embryos derived from Fmr13/Df(3R)Exel6265 females to below 25% for embryos from RpS131/+;Fmr13/Df(3R)Exel6265 mothers.
Homozygous mutant RpI135k16513 clone survival can be rescued by genetically reducing the growth of surrounding cells by making them heterozygous for a dominant Minute RpS131 mutant. In this case, RpI135k16513 mutant clones are recovered in all RpS131 heterozygous discs that are examined at 96hrs after clone induction, a time-point at which all clones are normally eliminated in a wild-type background. However, these clones colonise a significantly smaller area of RpS131/+ discs compared with wild-type clones (28.8% compared to 67.8% of the total disc area), indicating that they are still growth impaired. Compared to surrounding heterozygote RpS131 or wild-type cells, RpI135k16513 mutant clone cells exhibit no significant change in either cell size or cell-cycle phasing.
Transcript level and phenotype are restored to wild type by Δ2-3 mobilisation of the P{lacW} insertion demonstrating the mutation is caused by the insertion.