Two nucleotide substitutions near the exon 3/intron 3 junction: a G to C substitution at the terminal nucleotide of exon 3 (this is also the first nucleotide of an Ala codon in the wild type) and a G to A substitution five nucleotides downstream of the exon-intron junction. This results in a splicing defect such that intron three is included in the mRNA. This is predicted to result in a A458R amino acid replacement followed by a frameshift producing a premature stop codon 17 amino acids downstream.
G22652915C
G?C
A459P | Cyp6d2-PA
A458R
The two nucleotide substitutions in this mutant eliminate splicing of intron 3 and result in a A458R amino acid replacement followed by a frameshift producing a premature stop codon 17 amino acids downstream.
G22652910A
G?A
The two nucleotide substitutions in this mutant eliminate splicing of intron 3 and result in a A458R amino acid replacement followed by a frameshift producing a premature stop codon 17 amino acids downstream.
Mutant flies are sensitive to camptothecin but not to topotecan or ionising radiation.
Mutant flies are not sensitive to irinotecan, bleomycin, mechlorethamine (nitrogen mustard), methyl methanesulfonate, or hydroxyurea.
Cyp6d2SD is rescued by Cyp6d2+tTa
Cyp6d2+tTa rescues the camptothecin sensitivity of Cyp6d2SD flies.
The Cyp6d2SD allele is present in many publicly available stocks. It is not present in the D. melanogaster sequenced strain.
