Glutamine auxotrophs with mutations in a nitrogen regulatory gene, ntrC, that is near glnA.

Abstract

Some mutations to glutamine auxotrophy in the 86 unit region of the Salmonella chromosome lie within the nitrogen regulatory gene, ntrC, rather than the structural gene encoding glutamine synthetase, glnA, Assignment of mutations to ntrC is based on fine structure mapping by P22-mediated transduction and on complementation analysis. Strains with ntrC lesions that cause glutamine auxotrophy (NtrCrepressor) have very low levels of glutamine synthetase (lower than those of strains that completely lack ntrC function and comparable to those of strains that lack ntrA function). NtrCrep strains fail to increase synthesis of glutamine synthetase or several amino acid transport components under nitrogen limiting conditions. Thus, like ntrA strains, they appear to repress glnA transcription and fail to activate transcription of glnA or other nitrogen controlled genes. Mutations that suppress the glutamine requirement caused by NtrCrep lesions arise at high frequency; these mutations also suppress the glutamine requirement caused by ntrA lesions. Several suppressor mutations result in loss of function of ntrC.