Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 20, Issue 2, Pages 222-226Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2008.01.013
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Funding
- NIAID NIH HHS [R01 AI033600, P01 AI065858, P01 AI065858-01A1, R01 AI033600-11A2] Funding Source: Medline
- NIAMS NIH HHS [R01 AR051472, R01 AR051472-01] Funding Source: Medline
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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. elf2 alpha, elF4E-BP, elF4B, 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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