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Transcriptional regulation of stress-inducible genes in procaryotes

Takashi Yura, Kenji Nakahigashi, Masaaki Kanemori

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Abstract

In procaryotes such as Escherichia coli, transcriptional activation of heat shock genes in response to elevated temperature is caused primarily by transient increase in the amount of sigma 32 (rpoH gene product) specifically required for transcription from the heat shock promoters. The increase in sigma 32 level results from increased translation of rpoH mRNA and from stabilization of sigma 32 which is ordinarily very unstable. Some of the factors and cis-acting elements that constitute the complex regulatory circuits have been identified and characterized, but detailed mechanisms as well as nature of sensors and signals remain to be elucidated. Whereas this "classical" heat shock regulon (sigma 32 regulon) provides major protective functions against thermal stress, a second heat shock regulon mediated by sigma E (sigma 24) encodes functions apparently required under more extreme conditions, and is activated by responding to extracytoplasmic signals. These regulons mediated by minor sigma factors (sigma 32 in particular) appear to be conserved in most gram-negative bacteria, but not in gram-positive bacteria.

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In procaryotes such as Escherichia coli, transcriptional activation of heat shock genes in response to elevated temperature is caused primarily by transient increase in the amount of sigma 32 (rpoH gene product) specifically required for transcription from the heat shock promoters. The increase in sigma 32 level results from increased translation of rpoH mRNA and from stabilization of sigma 32 which is ordinarily very unstable. Some of the factors and cis-acting elements that constitute the complex regulatory circuits have been identified and characterized, but detailed mechanisms as well as nature of sensors and signals remain to be elucidated. Whereas this "classical" heat shock regulon (sigma 32 regulon) provides major protective functions against thermal stress, a second heat shock regulon mediated by sigma E (sigma 24) encodes functions apparently required under more extreme conditions, and is activated by responding to extracytoplasmic signals. These regulons mediated by minor sigma factors (sigma 32 in particular) appear to be conserved in most gram-negative bacteria, but not in gram-positive bacteria.

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Available abstract

In procaryotes such as Escherichia coli, transcriptional activation of heat shock genes in response to elevated temperature is caused primarily by transient increase in the amount of sigma 32 (rpoH gene product) specifically required for transcription from the heat shock promoters. The increase in sigma 32 level results from increased translation of rpoH mRNA and from stabilization of sigma 32 which is ordinarily very unstable. Some of the factors and cis-acting elements that constitute the complex regulatory circuits have been identified and characterized, but detailed mechanisms as well as nature of sensors and signals remain to be elucidated. Whereas this "classical" heat shock regulon (sigma 32 regulon) provides major protective functions against thermal stress, a second heat shock regulon mediated by sigma E (sigma 24) encodes functions apparently required under more extreme conditions, and is activated by responding to extracytoplasmic signals. These regulons mediated by minor sigma factors (sigma 32 in particular) appear to be conserved in most gram-negative bacteria, but not in gram-positive bacteria.

Key concepts: Gene, Genetics, Biology, Computational biology, Stress (linguistics), Philosophy, Linguistics

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