Further, since glnE has been reported to be an essential gene in other pathogens such as Mycobacterium tuberculosis [23,24] and we have been unable to construct a gonococcal glnE null mutant (data not presented), we posit that the opposing regulatory properties of MtrR on glnA and glnE likely serves to modulate the fidelity of glutamine biosynthesis during infection. This evidence concerns the gene MTRR and infection.