mei-9A1/mei-9A1 third instar larval brains exhibit increased frequency of cells with chromosome aberrations but without telomeric fusions compared to controls.
Similarly to wild-type third-instar larvae, X-ray irradiation of mei-9A1 mutants induces cell cycle arrest in wing imaginal disc cells.
When homozygous mutants are UV irradiated a complete ablation of the eye is seen due to an increase in apoptotic cell death. Light-induced photorepair partially rescues the eye phenotype.
Homozygotes are sensitive to methyl methanesulfonate and γ rays.
Homozygotes have an increased frequency of X chromosome non-disjunction.
Approximately 20-28% of embryos hatch. Approximately 18% of mus201D1 mei-9A1 double mutant embryos hatch. Homozygous larvae derived from homozygous mothers are 35.1 times more sensitive to methyl methanesulfonate and 5.5 times more sensitive to UV light than wild-type. Homozygous mei-9A1 or mei-9A1 mus201D1 embryonic cells in culture show no detectable unscheduled DNA synthesis (UDS) activity in response to methyl methanesulfonate, N-methyl-N-nitrosourea, X rays or UV light, over dose ranges in which wild-type cells show a strong dose-dependent UDS response.
Larvae show wild-type sensitivity to formaldehyde.
Homozygotes and hemizygotes show a higher frequency of spontaneous chromosome aberrations in neuroblast metaphases than wild-type larvae. The ratio of chromatid breaks to isochromatid breaks is 8.2-9.2. Approximately half of the breaks are heterochromatic and half are euchromatic. The breaks appear to be randomly distributed among the chromosomes. Breaks are 1.4-1.6 times more frequent in females than in males.
Hemizygous male larvae are sensitive to methyl methanesulfonate (MMS). They show sensitivity to ultra violet (UV) light and X rays. 28.4% of eggs laid by homozygous females develop into adults that eclose.
mutagen sensitive reduces exchange mitotic instability