Mutations exhibit a partial deficiency in the capacity to excise UV-induced pyrimidine dimers. In addition cells are defective in photorepair (FBrf0046353).
Cells derived from homozygous embryos are totally incapable of photorepair (light induced reversal of pyrimidine dimers) and partially deficient in excision repair.
Cells derived from homozygous embryos are deficient in photorepair: incapable of repairing UV-induced pyrimidine dimers after exposure to fluorescent illumination. Also there are some problems with excision repair. Since phr/phr larvae show little or no photoreactivation after exposure to short wavelength UV light, the phr+ function is thought to play a significant role in UV resistance.
Isolated from: Standard laboratory stocks.
Mutation is recessive.