Regulation of the alternative sigma factor σE during initiation, adaptation, and shutoff of the extracytoplasmic heat shock response in Escherichia coli

Sarah E. Ades, Irina L. Grigorova, Carol A. Gross

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

The alternative sigma factor σE is activated in response to stress in the extracytoplasmic compartment of Escherichia coli. Here we show that σE activity increases upon initiation of the stress response by a shift to an elevated temperature (43°C) and remains at that level for the duration of the stress. When the stress is removed by a temperature downshift, σE activity is strongly repressed and then slowly returns to levels seen in unstressed cells. We provide evidence that information about the state of the cell envelope is communicated to σE primarily through the regulated proteolysis of the inner membrane anti-sigma factor RseA, as the degradation rate of RseA is correlated with the changes in σE activity throughout the stress response. However, the relationship between σE activity and the rate of degradation of RseA is complex, indicating that other factors may cooperate with RseA and serve to fine-tune the response.

Original languageEnglish (US)
Pages (from-to)2512-2519
Number of pages8
JournalJournal of bacteriology
Volume185
Issue number8
DOIs
StatePublished - Apr 1 2003

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Heat-Shock Response
Escherichia coli
Sigma Factor
Temperature
Proteolysis
Membranes
sporulation-specific sigma factors

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Molecular Biology

Cite this

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Regulation of the alternative sigma factor σE during initiation, adaptation, and shutoff of the extracytoplasmic heat shock response in Escherichia coli. / Ades, Sarah E.; Grigorova, Irina L.; Gross, Carol A.

In: Journal of bacteriology, Vol. 185, No. 8, 01.04.2003, p. 2512-2519.

Research output: Contribution to journalArticle

TY - JOUR

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AB - The alternative sigma factor σE is activated in response to stress in the extracytoplasmic compartment of Escherichia coli. Here we show that σE activity increases upon initiation of the stress response by a shift to an elevated temperature (43°C) and remains at that level for the duration of the stress. When the stress is removed by a temperature downshift, σE activity is strongly repressed and then slowly returns to levels seen in unstressed cells. We provide evidence that information about the state of the cell envelope is communicated to σE primarily through the regulated proteolysis of the inner membrane anti-sigma factor RseA, as the degradation rate of RseA is correlated with the changes in σE activity throughout the stress response. However, the relationship between σE activity and the rate of degradation of RseA is complex, indicating that other factors may cooperate with RseA and serve to fine-tune the response.

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