Mutation is within the C-terminal end of the kinase domain.
Amino acid replacement: W1134term.
G11361948A
W1134term | hop-PA
W1134term
G to A nucleotide change at the second or third position of the wild type Trp codon leads to a nonsense mutation (exact site of mutation unspecified). The mutation was annotated at the second base of the codon.
abnormal immune response (with hop25)
hop32/hop25 mutant flies die more rapidly than do wild-type controls following Drosophila C virus (DCV) infection, and contain about 10-fold more virus.
Compared with wild-type, hop32/hop25 mutant flies show decreased survival and contain significantly more virus particles when injected with Cricket Paralysis Virus (CrPV).
The concentration of circulating hemocytes in mutant larvae and the distribution of the different blood cell types is not different from that of controls.
hop25/hop32 females can have eyes that are smaller in the dorso-ventral axis with significantly fewer ommatidia compared to wild-type. Ommatidia are arranged irregularly and duplicated bristles are seen. hop25/hop32 females with an eyeless phenotype with a concomitant duplication of the antenna can also be seen.
50% viable in transheterozygous combination with hop25.
Paternal rescue of the maternal effect. Germline clone analysis demonstrates that embryos have one abdominal segment missing and A4 appears wider than wild type, and partial or complete fusion of T1 and T2.
hop32/hop25 has partially lethal phenotype, enhanceable by upd1YM55
Scer\GAL4en-e16E, Socs44AUAS.cRa, hop32/hop25 has lethal phenotype
hop32/hop25 has wing vein | ectopic phenotype, non-suppressible by Df(2R)Drlrv18/+
The penetrance of the ectopic wing vein phenotype seen in hop25/hop32 animals (98%) is decreased by Df(2R)CA53/+ (46%) or Df(2R)NCX10/+ (58%), but is not significantly decreased by Df(2R)Drlrv18/+ (87%).
Voelker.
Fully complement hop25.