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The adaptation of mRNA stability to environmental changes is a means of cells to adjust the level of gene expression. The  Escherichia coli ompA  mRNA has served as one of the paradigms for regulated mRNA decay in prokaryotes. The stability of the transcript is known to be correlated inversely with the bacterial growth rate. Thus, the regulation of  ompA  mRNA stability meets the physiological needs to adjust the level of  ompA  expression to the rate of cell division. Recently, host factor I (Hfq/HF1) was shown to be involved in the regulation of  ompA  mRNA stability under slow growth conditions. Here, we present the first direct demonstration that 30S ribosomes bound to the  ompA  5′-UTR protect the transcript from RNase E cleavage in vitro. However, the 30S protection was found to be abrogated in the presence of Hfq. Toeprinting and in vitro translation assays revealed that translation of  ompA  is repressed in the presence of Hfq. These in vitro studies are corroborated by in vivo expression studies demonstrating that the reduced synthesis rate of OmpA effected by Hfq results in functional inactivation of the ompA mRNA. The data are discussed in terms of a model wherein Hfq regulates the stability of  ompA  mRNA by competing with 30S ribosomes for binding to the  ompA  5′-UTR.

Hfq (HF1) stimulates ompA mRNA decay by interfering with ribosome binding