Homozygous Mnn1e200 mutants (Df(2L)Mnn1e200 mutants in which milt function is rescued by expression of the milt+22 transgene) show a greater sensitivity to ionizing radiation when exposed as second and third instar larvae compared to wild-type larvae. As first instar larvae, these Mnn1e200 mutants show increased sensitivity to the DNA cross-linking agents nitrogen mustard and cisplatinum at room temperature and 29oC, and increased sensitivity to diepoxybutane and mitomycin C at 29oC but not at room temperature. These mutants display similar sensitivity to wild-type larvae when exposed to methyl methanosulphonate, hydroxyurea and 2-Acetylaminofluorene.
Mnn1e200 mutant cells are able to arrest normally at the G2/M transition after irradiation and show indistinguishable levels of apoptosis to controls.
Mnn1e200 is a non-enhancer of visible | chemical conditional phenotype of Fancd2RNAi.UAS, Scer\GAL4ey.PU
Mnn1e200 is a non-suppressor of visible | chemical conditional phenotype of Fancd2RNAi.UAS, Scer\GAL4ey.PU
Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has chemical sensitive phenotype
Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has neoplasia | conditional phenotype
Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has visible | chemical conditional phenotype
Mnn1e200 is a non-enhancer of eye | chemical conditional phenotype of Fancd2RNAi.UAS, Scer\GAL4ey.PU
Mnn1e200 is a non-suppressor of eye | chemical conditional phenotype of Fancd2RNAi.UAS, Scer\GAL4ey.PU
Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has eye | chemical conditional phenotype
A Mnn1e200 mutant background enhances the rate of eye tumor formation in response to nitrogen mustard compared to wtsx1/+ mutant controls.
The presence of homozygous Mnn1e200 does not alter the rough eye phenotype seen in flies expressing Fancd2dsRNA.Scer\UAS under the control of Scer\GAL4ey.PU in response to the cross-linking agent cisplatinum.
Homozygous Mnn1e200 mutants (Df(2L)Mnn1e200 mutants in which milt function is rescued by expression of the milt+22 transgene) that have a wtsx1/+ background show a two-fold greater number of tumorigenic foci than wtsx1/+ single mutants. After treatment with ionizing radiation, the number of tumorigenic foci is two to three times higher in these mutants than in controls and is 7-fold higher after treatment with nitrogen mustard.
The viability of Mnn1e200 mutants (Df(2L)Mnn1e200 mutants in which milt function is rescued by expression of the milt+22 transgene) is not affected by a snw background.