G to A mutation in the first nucleotide of the third intron, resulting in a non-functional splice donor site. RT-PCR analysis shows that the third intron is retained, and the presence of in an in-frame stop codon at the end of the third intron results in a truncated protein, lacking known functional domains. All three splice variants identified are affected by the mutation.
G19523435A
G to A mutation in the first nucleotide of the third intron, resulting in a non-functional splice donor site.
Homozygous posterior follicle cells are smaller and have much smaller nuclei than their neighbouring wild-type cells in mosaic egg chambers. Homozygous follicle cell clones fail to undergo the switch from mitotic cycles to endocycles, with mitotic markers present after stage 6. This proliferation phenotype is more pronounced in the posterior follicle cells.
CoRest[+]/CoRestGF60 is an enhancer of visible | dominant phenotype of Delta7
CoRest[+]/CoRestGF60, NXK11 has visible | dominant phenotype
CoRest[+]/CoRestGF60 is an enhancer of wing vein phenotype of Delta7
CoRest[+]/CoRestGF60, NXK11 has wing vein phenotype
CoRest[+]/CoRestGF60, NXK11 has wing blade phenotype
The wing defects seen in Dl7/+ flies are enhanced by CoRestGF60/+: the extent of thickening and deltas at the wing veins is increased and in some cases severe wing blistering is seen.
CoRestGF60/NXK11 transheterozygotes show thickened wing veins and deltas. Wing blistering is occasionally seen.
CoRestGF60 is rescued by Scer\GAL4e22c/CoRestUASp.Tag:HA