Open Close
Reference
Citation
Rodriguez, A., Chen, P., Oliver, H., Abrams, J.M. (2002). Unrestrained caspase-dependent cell death caused by loss of Diap1 function requires the Drosophila Apaf-1 homolog, Dark.  EMBO J. 21(9): 2189--2197.
FlyBase ID
FBrf0147000
Publication Type
Research paper
Abstract

In mammals and Drosophila, apoptotic caspases are under positive control via the CED-4/Apaf-1/Dark adaptors and negative control via IAPs (inhibitor of apoptosis proteins). However, the in vivo genetic relationship between these opposing regulators is not known. In this study, we demonstrate that a dark mutation reverses catastrophic defects seen in Diap1 mutants and rescues cells specified for Diap1- regulated cell death in development and in response to genotoxic stress. We also find that dark function is required for hyperactivation of caspases which occurs in the absence of Diap1. Since the action of dark is epistatic to that of Diap1, these findings demonstrate that caspase-dependent cell death requires concurrent positive input through Apaf-1-like proteins together with disruption of IAP-caspase complexes.

PubMed ID
PubMed Central ID
PMC125994 (PMC) (EuropePMC)
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    EMBO J.
    Title
    The EMBO Journal
    Publication Year
    1982-
    ISBN/ISSN
    0261-4189
    Data From Reference
    Alleles (8)
    Genes (5)
    Insertions (2)
    Transgenic Constructs (3)