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Mol Cell. 2018 Apr 19;70(2):274-286.e7. doi: 10.1016/j.molcel.2018.02.035. Epub 2018 Apr 5.

A Stress Response that Monitors and Regulates mRNA Structure Is Central to Cold Shock Adaptation.

Author information

1
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA 94158, USA.
2
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA; Graduate Group in Biophysics, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute of Quantitative Biology, University of California, San Francisco, San Francisco, CA 94158, USA.
3
Department of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute of Quantitative Biology, University of California, San Francisco, San Francisco, CA 94158, USA; Center for RNA Systems Biology, University of California, San Francisco, San Francisco, CA 94158, USA.
4
Department of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute of Quantitative Biology, University of California, San Francisco, San Francisco, CA 94158, USA; Center for RNA Systems Biology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: gwli@mit.edu.
5
Department of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute of Quantitative Biology, University of California, San Francisco, San Francisco, CA 94158, USA; Center for RNA Systems Biology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: jonathan.weissman@ucsf.edu.
6
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute of Quantitative Biology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: cgrossucsf@gmail.com.

Abstract

Temperature influences the structural and functional properties of cellular components, necessitating stress responses to restore homeostasis following temperature shift. Whereas the circuitry controlling the heat shock response is well understood, that controlling the E. coli cold shock adaptation program is not. We found that during the growth arrest phase (acclimation) that follows shift to low temperature, protein synthesis increases, and open reading frame (ORF)-wide mRNA secondary structure decreases. To identify the regulatory system controlling this process, we screened for players required for increased translation. We identified a two-member mRNA surveillance system that enables recovery of translation during acclimation: RNase R assures appropriate mRNA degradation and the Csps dynamically adjust mRNA secondary structure to globally modulate protein expression level. An autoregulatory switch in which Csps tune their own expression to cellular demand enables dynamic control of global translation. The universality of Csps in bacteria suggests broad utilization of this control mechanism.

KEYWORDS:

DMS-seq; RNA regulation; RNA secondary structure; cold shock; cold shock proteins; ribosome profiling; translation

PMID:
29628307
PMCID:
PMC5910227
DOI:
10.1016/j.molcel.2018.02.035
[Indexed for MEDLINE]
Free PMC Article

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