The adaptation of mRNA stability to environmental changes is a means of cel
ls to adjust the level of gene expression. The Escherichia coli ompA mRNA h
as served as one of the paradigms for regulated mRNA decay in prokaryotes.
The stability of the transcript is known to be correlated inversely with th
e 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 involve
d in the regulation of ompA mRNA stability under slow growth conditions. He
re, we present the first direct demonstration that 30S ribosomes bound to t
he ompA 5'-UTR protect the transcript from RNase E cleavage in vitro. Howev
er, the 30S protection was found to be abrogated in the presence of Hfq. To
eprinting and in vitro translation assays revealed that translation of ompA
is repressed in the presence of Hfq. These in vitro studies are corroborat
ed by in vivo expression studies demonstrating that the reduced synthesis r
ate 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 o
mpA 5'-UTR.