First published online August 26, 2004
Journal of Cell Science 117, 1905e (2004)
© The Company of Biologists Limited
Stressed about death
When chemically or physically stressed, cells have two options: they can try to repair the damage by activating cellular defense mechanisms, or they can throw in the towel and turn on apoptosis. Guido Kroemer and colleagues now describe an unexpected crosstalk between apoptosis and the formation of cytoplasmic stress granules (SGs), a cellular defense mechanism (see p. 4461). SGs are dynamic foci at which stalled translation initiation complexes accumulate in response to cellular stress. The authors show that apoptosis-inducing factor (AIF)-depleted HeLa cells nucleate SG signature proteins more efficiently in response to redox stress than do AIF-positive cells. AIF must be present in the mitochondria to repress SG formation – it must be nuclear to have its pro-apoptotic effects – and different AIF domains are required for SG inhibition and for its apoptogenic activity. The authors also report that AIF modulates SG formation by regulating glutathione levels and speculate that other pro-apoptotic proteins may, like AIF, both stimulate apoptosis and blunt adaptive stress responses.
Related articles in JCS:
- Regulation of cytoplasmic stress granules by apoptosis-inducing factor
- Céline Candé, Nicola Vahsen, Didier Métivier, Hélène Tourrière, Karim Chebli, Carmen Garrido, Jamal Tazi, and Guido Kroemer
JCS 2004 117: 4461-4468.
[Abstract]
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