Myc inhibits JNK-mediated cell death in vivo.
The proto-oncogene Myc is well known for its roles in promoting cell growth, proliferation and apoptosis. However, in this study, we found from a genetic screen that Myc inhibits, rather than promotes, cell death triggered by c-Jun N-terminal kinase (JNK) signaling in Drosophila. Firstly, expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK signaling-induced cell death. Secondly, dMyc impedes physiologically activated JNK pathway-mediated cell death. Thirdly, loss of dMyc triggers JNK pathway activation and JNK-dependent cell death. Finally, the mammalian cMyc gene, when expressed in Drosophila, impedes activated JNK signaling-induced cell death. Thus, besides its well-studied apoptosis promoting function, Myc also antagonizes JNK-mediated cell death in Drosophila, and this function is likely conserved from fly to human.
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Jiuhong
J
Huang
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Yu
Y
Feng
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Xinhong
X
Chen
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China. lwz@tongji.edu.cn.
Wenzhe
W
Li
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China. lei.xue@tongji.edu.cn.
Lei
L
Xue
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D054910:Compound Eye, Arthropod / Q000166:cytology / Q000196:embryology / Q000254:growth & development; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D029721:Drosophila Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D004331:Drosophila melanogaster / Q000166:cytology / Q000235:genetics*; D005260:Female; D018507:Gene Expression Regulation, Developmental; D005813:Genes, Synthetic; D016259:Genes, myc; D006801:Humans; D007814:Larva; D020935:MAP Kinase Signaling System / Q000235:genetics*; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology; D009024:Morphogenesis; D020033:Protein Isoforms / Q000235:genetics / Q000502:physiology; D000090063:Proto-Oncogene Mas; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000502:physiology; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D013045:Species Specificity; D013909:Thorax / Q000166:cytology / Q000196:embryology / Q000254:growth & development; D014157:Transcription Factors / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D014921:Wings, Animal / Q000166:cytology / Q000196:embryology / Q000254:growth & development
D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; C557617:GAL4 protein, Drosophila; C000715470:MAS1 protein, human; C489427:MYC protein, human; D008565:Membrane Proteins; C102284:Myc protein, Drosophila; D020033:Protein Isoforms; D000090063:Proto-Oncogene Mas; D016271:Proto-Oncogene Proteins c-myc; D011993:Recombinant Fusion Proteins; D014157:Transcription Factors; C464573:egr protein, Drosophila
Cell death; Drosophila; JNK pathway; Myc