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Reprogramming mRNA translation during stress.

Satoshi Yamasaki1, Paul Anderson

  • 1Harvard Medical School, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Smith 652, One Jimmy Fund Way, Boston, MA 02115, United States.

Current Opinion in Cell Biology
|March 22, 2008
PubMed
Summary
This summary is machine-generated.

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Mammalian cells survive stress by reprogramming protein translation. This process inhibits basic protein production while favoring repair enzymes, conserving energy and repairing damage.

Area of Science:

  • Molecular biology
  • Cellular stress response
  • Protein synthesis regulation

Background:

  • Cellular survival under adverse conditions necessitates significant adaptive mechanisms.
  • Protein translation is a key cellular process that is tightly regulated.
  • Stress conditions trigger specific signaling pathways that impact cellular functions.

Purpose of the Study:

  • To elucidate the mechanisms by which mammalian cells reprogram protein translation during stress.
  • To understand how stress granules contribute to mRNA fate.
  • To identify the pathways involved in selective translation of repair enzymes.

Main Methods:

  • Analysis of stress-activated kinases and their targets in protein translation initiation.
  • Investigation of mRNA localization and dynamics within stress granules.

Related Experiment Videos

  • Characterization of internal ribosome entry site (IRES)-dependent and -independent translation mechanisms under stress.

    • Main Results:

    • Stress-activated kinases reprogram translation by targeting initiation factors like eIF2alpha and eIF4E-BP.
    • Untranslated mRNAs accumulate in stress granules for triage (storage, reinitiation, or decay).
    • Selective translation of repair enzyme mRNAs is maintained through specific mechanisms.

    Conclusions:

    • Cellular stress induces a coordinated reprogramming of mRNA translation and decay.
    • This reprogramming conserves energy, preserves vital mRNAs, and facilitates repair of cellular damage.
    • The stress response optimizes protein synthesis for survival and recovery.