Translocation of <i>C. elegans</i> CED-4 to Nuclear Membranes During Programmed Cell Death
SciencePublished 25 February 2000
Fangli Chen, Bradley M. Hersh, Barbara Conradt, Zheng Zhou, Dieter Riemer, Yosef Gruenbaum
Citations242
SJR quartileQ1
SJR score10.42
SNIP6.62
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TL;DR
CED-4 translocation induced by the cell-death activator EGL-1 was blocked by a gain-of-function mutation in cED-9 but was not dependent on ced-3 function, suggesting that CED- 4 translocation precedes caspase activation and the execution phase of programmed cell death.
Abstract
The Caenorhabditis elegans Bcl-2-like protein CED-9 prevents programmed cell death by antagonizing the Apaf-1-like cell-death activator CED-4. Endogenous CED-9 and CED-4 proteins localized to mitochondria in wild-type embryos, in which most cells survive. By contrast, in embryos in which cells had been induced to die, CED-4 assumed a perinuclear localization. CED-4 translocation induced by the cell-death activator EGL-1 was blocked by a gain-of-function mutation in ced-9 but was not dependent on ced-3 function, suggesting that CED-4 translocation precedes caspase activation and the execution phase of programmed cell death. Thus, a change in the subcellular localization of CED-4 may drive programmed cell death.
Keywords
Biochemistry, Genetics and Molecular Biology
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