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The surface-exposed NadA adhesin produced by a subset of capsular serogroup B strains of  Neisseria meningitidis  is currently being considered as a vaccine candidate to prevent invasive disease caused by a hypervirulent lineage of meningococci. Levels of NadA are known to be controlled by both transcriptional regulatory factors and a component of human saliva, 4-hydroxyphenylacetic acid. Herein, we confirmed the capacity of a DNA-binding protein termed FarR to negatively control  nadA  expression. We also found that a known transcriptional regulator of  farR  in  N .  gonorrhoeae  termed MtrR can have a negative regulatory impact on  farR  and  nadA  expression, especially when over-expressed. MtrR-mediated repression of  nadA  was found to be direct, and its binding to a target DNA sequence containing the  nadA  promoter influenced formation and/or stability of FarR:: nadA  complexes. The complexity of the multi-layered regulation of  nadA  uncovered during this investigation suggests that  N. meningitidis  modulates NadA adhesin protein levels for the purpose of interacting with host cells yet avoiding antibody directed against surface exposed epitopes.

plos one

MtrR Control of a Transcriptional Regulatory Pathway in Neisseria meningitidis That Influences Expression of a Gene (nadA) Encoding a Vaccine Candidate