Amino acid replacement: W87term.
G13389613A
W87term | Poc1-PA; W87term | Poc1-PB
W87term
G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Homozygous Poc1W87X adults display morphological sperm defects (immotile spermatozoa with abnormal axoneme structure, shorter giant centriole compared to controls) but their locomotor behavior appears unaffected (suggesting sensory cilia function is not perturbed).
Expression of ana2Ubi.C.GFP in combination with Sas-6Ubi.P.GFP leads to formation of procentriolar ectopic particles while their expression in Poc1W87X homozygous background leads to structural defects in procentriolar ectopic particles such as fragmented tubule-like structures and electron-dense material in mature primary spermatocytes.
Poc1W87X is rescued by Poc1UAS.B.GFP/Poc1UAS.A.GFP/Scer\GAL4bam.PU
Poc1W87X is partially rescued by Poc1UAS.A.GFP/Scer\GAL4bam.PU
Poc1W87X is not rescued by Poc1UAS.B.GFP/Scer\GAL4bam.PU
Expression of Poc1UAS.A.GFP alone under the control of Scer\GAL4bam.PU in the Poc1W87X mutant background rescues the sperm motility defect characteristic for Poc1W87X males but not the reduced size of the giant centriole in the sperm cells. Expression of Poc1UAS.B.GFP alone cannot rescue either of the phenotypes but simultaneous expression of both Poc1UAS.A.GFP and Poc1UAS.B.GFP using the same driver rescues both phenotypes and the progeny of these males show nearly normal embryonic development rate compared (unlike the embryos fathered by Poc1W87X mutants expressing only Poc1UAS.A.GFP which are severely delayed).