Point mutation in splice acceptor site.
Point mutation.
A4516321T
Point mutation in the splice acceptor site immediately before the initiating ATG.
Heterozygous adults eclose with a delay of about a day compared to control flies. RpL3845-72/RpL38NC21 animals show 5% viability. These animals also show notches on the wing margin.
No Minute phenotype.
Chie5.5, RpL38[+]/RpL3845-72 has visible | dominant phenotype
RpL38[+]/RpL3845-72, mamg2.1 has visible | dominant phenotype
RpL3845-72, ct2s has visible | dominant phenotype
RpL38[+]/RpL3845-72, vg1 has visible | dominant phenotype
RpL3845-72 is an enhancer of phenotype of mamg2.1
RpL3845-72 is an enhancer of phenotype of vg1
RpL3845-72 is an enhancer of wing phenotype of ct53d
RpL3845-72 is an enhancer of wing phenotype of Nnd-1
RpL3845-72 is an enhancer of phenotype of Chie5.5
RpL3845-72 is a non-enhancer of phenotype of wgl-17
RpL3845-72 is a non-enhancer of phenotype of ap56f
RpL3845-72 is a non-enhancer of wing phenotype of ctL32, su(Hw)e2
RpL3845-72 is a suppressor of wing vein phenotype of NAx-E2
RpL3845-72 is a suppressor of eye phenotype of Nspl-1
Chie5.5, RpL38[+]/RpL3845-72 has wing phenotype
RpL3845-72, vg[+]/vg1 has wing phenotype
RpL3845-72, mamg2.1/mam[+] has wing phenotype
Chi[+]/Chie5.5, RpL3845-72 has wing phenotype
RpL3845-72, ct2s has wing phenotype
RpL38[+]/RpL3845-72, vg1 has wing phenotype
RpL38[+]/RpL3845-72, mamg2.1 has wing phenotype
Hilliker.
Separable from: a Pin mutation.