Abstract
Synthesis of the colicin I receptor protein, encoded by the cir gene, was determined to be sensitive to control by the catabolite repression regulatory system. Under both high- and low-iron conditions for growth, mutants unable to produce cyclic AMP (cAMP) (cya) or functional cAMP receptor protein (crp) exhibited decreased membrane levels of the receptor relative to those of the wild-type strain. Exogenous addition of cAMP to the cya mutant restored maximal expression. cAMP-dependent changes in steady-state levels of cir mRNA suggested that the effect is mediated by control of transcript synthesis or stability. Potential mechanisms for regulation were examined by deletion and sequence analysis.
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