Translocation of C. elegans CED-4 to nuclear membranes during programmed cell death

被引:195
作者
Chen, FL
Hersh, BM
Conradt, B
Zhou, Z
Riemer, D
Gruenbaum, Y
Horvitz, HR
机构
[1] MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA
[2] Max Planck Inst Biophys Chem, Dept Biochem, D-37016 Gottingen, Germany
[3] Hebrew Univ Jerusalem, Inst Life Sci, Dept Genet, IL-91904 Jerusalem, Israel
关键词
D O I
10.1126/science.287.5457.1485
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1485 / 1489
页数:5
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