A clinical strain of Escherichia coli, C16, that overproduces the ampC beta-lactamase was isolated. A 203-bp DNA segment from this strain, including the promoter and attenuator region of the ampC structural gene, was sequenced. A comparison with the corresponding sequence of E. coli K12 revealed four base pair differences between the ampC segments from these strains. DNA sequence data and in vitro transcription indicated that the ampC promoter in the clinical isolate was displaced 5 bp upstream of the promotor defined in the E. coli K12 strain. Like the ampC gene of E. coli K12, the ampC gene from the clinical isolate was metabolically regulated. However, the increase in the specific amount of beta-lactamase relative to the increase in specific growth rate was much higher in the clinical isolate. These data imply that the growth rate-dependent anti-termination acting on the ampC attenuator in vivo is more pronounced in the clinical E. coli isolate than in E. coli K12. A possible molecular mechanism for this is discussed.