In vivo p53 function is indispensable for DNA damage-induced apoptotic signaling in Drosophila.
p53 is a representative tumor suppressor whose dysfunction is a major cause of human cancer syndrome. Here we isolated flies lacking Dmp53, which encodes the single Drosophila orthologue of mammalian p53 family. Dmp53 null mutants well developed into adults, only displaying mild defects in longevity and fertility. However, genomic stability and viability of Dmp53 mutants dramatically decreased upon ionizing irradiation. Moreover, mutating Dmp53 abolished irradiation-induced apoptosis and reaper induction. These results indicate that Dmp53 is a central component of DNA damage-dependent apoptotic signaling.
Lee
Jun Hee
JH
National Creative Research Initiatives Center for Cell Growth Regulation, Korea Advanced Institute of Science and Technology, Taejon 305-701, South Korea.
Lee
Eunji
E
Park
Jeehye
J
Kim
Euysoo
E
Kim
Jaeseob
J
Chung
Jongkyeong
J
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D020169:Caspases / Q000378:metabolism; D002453:Cell Cycle / Q000235:genetics; D004249:DNA Damage / Q000502:physiology*; D004330:Drosophila / Q000196:embryology / Q000502:physiology* / Q000528:radiation effects; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism* / Q000528:radiation effects; D004625:Embryo, Nonmammalian / Q000528:radiation effects; D004789:Enzyme Activation; D005260:Female; D005298:Fertility / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D008136:Longevity / Q000235:genetics; D009154:Mutation; D011401:Promoter Regions, Genetic; D011839:Radiation, Ionizing; D015398:Signal Transduction; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53; D014921:Wings, Animal / Q000254:growth & development / Q000473:pathology / Q000528:radiation effects
D029721:Drosophila Proteins; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; C474203:p53 protein, Drosophila; C086973:rpr protein, Drosophila; D020169:Caspases