Normal levels of induced mutations after treatment with the ethylating agents ENU and EMS and enhanced levels after treatment with methylating agents MMU and MMS, a similar phenotype to that of mutants at mus201.

Homozygous larvae derived from homozygous females show greater sensitivity to methyl methanesulfonate (MMS) than homozygous larvae derived from heterozygous females.

Fecundity of homozygous females reduced, although partial rescue effected by fertilization with sperm carrying mus205⁺. X-chromosome disjunction regular; slight increase in the number of fourth-chromosome exceptions noted.

Flies are sensitive to ether anaesthesia. Flies are resistant to γ-ray knockdown.

Displays hypermutability to alkylating agents; defective both in alkylation and UV excision repair pathways.

Cells derived from homozygous embryos are deficient in photorepair and have defects in postreplication repair.

Cells derived from homozygous embryos synthesise DNA at a reduced rate both from an undamaged template and after UV irradiation compared to wild-type cells. Homozygous larval brain ganglia have a reduced ability to synthesise DNA after exposure to N-acetoxy-2-acetylaminofluorene compared to wild-type.

Homozygous larvae are sensitive to UV light and methyl methanesulfonate, but not to X rays, formaldehyde or nitrogen mustard. Homozygous females have reduced reproductive capacity, which can be partially rescued when homozygous oocytes are fertilised by wild-type sperm.

Larval survival hypersensitive to exposure to methyl methanesulfonate and ultraviolet light, moderately sensitive to benzo^apyrene, but not to formaldehyde, nitrogen mustard or ionizing radiation. Partially deficient in excision repair and postreplication repair.