Translocation of C. elegans CED-4 to Nuclear Membranes During Programmed Cell Death

作者：Fangli Chen, Bradley M. Hersh, Barbara Conradt, Zheng Zhou, Dieter Riemer, Yosef Gruenbaum, H. Robert Horvitz · 发表于：Science · 年份：2000 · DOI：10.1126/science.287.5457.1485 · 被引用次数：246 · 研究领域：Genetics, Aging, and Longevity in Model Organisms、Cell death mechanisms and regulation、Mitochondrial Function and Pathology

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.