Abstract
Jun amino-terminal kinase (JNK) mediates a physiological stress signal that leads to cell death. However, the role of the JNK pathway in intrinsic cell death execution mechanisms is largely unknown. In a genetic screen for dominant suppressors of Reaper (Rpr)-induced cell death, we identified Drosophila chromosomal regions that contain genes which are homologous to apoptosis signal-regulating kinase (ASK1) and Drosophila tumor necrosis factor receptor-associated factor 1 (DTRAF1). We present evidence that the killer signal initiates the JNK pathway via proteasome-mediated degradation of Drosophila inhibitor of apoptosis protein 1 (DIAP1) to promote cell death.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis / genetics*
-
Chromosomes / genetics
-
Drosophila / genetics*
-
Drosophila / physiology
-
Drosophila Proteins / genetics*
-
Drosophila Proteins / metabolism
-
Genes, Insect
-
Genetic Testing
-
Inhibitor of Apoptosis Proteins
-
JNK Mitogen-Activated Protein Kinases / metabolism*
-
MAP Kinase Kinase Kinase 5 / genetics
-
Proteasome Endopeptidase Complex / metabolism
-
Signal Transduction / genetics
-
Suppression, Genetic / genetics*
Substances
-
DIAP1 protein, Drosophila
-
Drosophila Proteins
-
Inhibitor of Apoptosis Proteins
-
rpr protein, Drosophila
-
JNK Mitogen-Activated Protein Kinases
-
MAP Kinase Kinase Kinase 5
-
Proteasome Endopeptidase Complex