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A novel DNA element that controls bacterial heat shock gene expression
Author(s) -
Narberhaus Franz,
Käser Roman,
Nocker Andreas,
Hennecke Hauke
Publication year - 1998
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1998.00794.x
Subject(s) - operon , derepression , biology , repressor , transcription (linguistics) , promoter , gene , microbiology and biotechnology , heat shock protein , mutant , cold shock domain , hspa4 , gal operon , psychological repression , gene expression , genetics , hsp70 , rna , linguistics , philosophy
The hspArpoH 1 and hspBCdegP heat shock operons of Bradyrhizobium japonicum are preceded by a novel, conserved DNA element of approximately 100 bp, which is responsible for the temperature‐regulated transcription of their σ 70 ‐type promoters. We designated this motif ROSE for repression of heat shock gene expression and found additional ROSE elements upstream of two newly identified heat shock operons. A critical core region in the hspA ‐associated ROSE 1 was defined by introducing insertions or deletions. While four mutants retained the ability to repress transcription of the hspArpoH 1 operon, five deletion mutants produced elevated hspA mRNA levels under low‐temperature growth conditions. Derepression was confirmed by increased RpoH 1 levels in non‐heat‐shocked cells from one of these mutants and by strains that contained a translational hspA – lacZ fusion associated with mutated ROSE 1 elements. The hspArpoH 1 operon was efficiently transcribed in vitro , and a deletion of ROSE 1 did not impair this activity. Gel retardation experiments demonstrated that a protein in non‐heat‐shocked cells specifically binds to the intact ROSE 1 element but not to a mutated element lacking the core region. Taken together, these results indicate that a central region of ROSE serves as a binding site for a repressor protein under standard growth conditions in order to prevent the undesired transcription of heat shock genes.