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Curr Opin Cell Biol. 2008 Apr;20(2):222-6. doi: 10.1016/ Epub 2008 Mar 20.

Reprogramming mRNA translation during stress.

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Harvard Medical School, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Smith 652, One Jimmy Fund Way, Boston, MA 02115, United States.


The survival of mammalian cells exposed to adverse environmental conditions requires a radical reprogramming of protein translation. Stress-activated kinases target components of the initiation machinery (e.g. eIF2alpha, eIF4E-BP, eIF4B, and ribosomal protein S6) to inhibit the translation of 'housekeeping' proteins and promote the translation of repair enzymes. Accumulating untranslated mRNA is concentrated at stress granules where it is sorted and triaged to sites of storage, reinitiation, or decay. At the same time, the translation of mRNAs encoding repair enzymes is selectively preserved by both internal ribosome entry site-dependent and -independent mechanisms. In combination, these stress-activated processes coordinately reprogram mRNA translation and decay in a way that conserves anabolic energy, preserves essential mRNAs, and promotes the repair of stress-induced molecular damage.

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