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First published online August 26, 2004

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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.

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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] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?