A 1,026-bp open reading frame sharing significant similarity with queA, which encodes a predicted S-adenosylmethionine:tRNA ribosyltransferase-isomerase responsible for queosine modification of tRNAs, was found immediately 5' of the gene for the transcriptional activator (ArcR) of the arginine deiminase system (ADS) operon of Streptococcus gordonii. The role of QueA in bacterial physiology is enigmatic, but loss of QueA has been shown to compromise stationary-phase survival or virulence in certain enteric bacteria. Interestingly, S. gordonii appears to be unique among ADS-positive bacteria in the linkage of queA with the ADS genes. A putative sigma(70) promoter (p(queA); TTGCCA-N(21)-TATAAT) was mapped 5' of queA by primer extension, and queA and arcR were shown to be cotranscribed. The expression from p(queA) was found to be constitutive under all conditions tested, but the expression of p(arcA), which drives the expression of the arc structural genes, was enhanced in stationary phase and could be induced by low pH and arginine. QueA and CcpA acted repressively on arc transcription, but neither QueA-deficient strains nor CcpA-deficient strains showed significant differences in arginine deiminase enzyme activities compared with the wild-type strain. The growth rate of a QueA-deficient strain did not differ significantly from that of the parental strain, but the QueA-deficient strain did not compete well with the wild-type during serial passage. In addition to the finding that ADS expression can be regulated separately by growth phase and pH, a significant linkage between the ADS, translational efficiency modulated by QueA, and post-exponential-phase survival of S. gordonii was found.