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S igma factor RpoN (σ 54 ) regulates pilE transcription in commensal N eisseria elongata
Author(s) -
Rendón María A.,
Hockenberry Alyson M.,
McManus Steven A.,
So Magdalene
Publication year - 2013
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12350
Subject(s) - biology , commensalism , transcription (linguistics) , transcription factor , rpon , pilus , pilin , microbiology and biotechnology , repressor , genetics , trans acting , gene , bacteria , escherichia coli , promoter , gene expression , mutant , linguistics , philosophy
Summary Human‐adapted N eisseria includes two pathogens, N eisseria gonorrhoeae and N eisseria meningitidis , and at least 13 species of commensals that colonize many of the same niches as the pathogens. The T ype IV pilus plays an important role in the biology of pathogenic N eisseria . In these species, S igma factor RpoD (σ 70 ), I ntegration H ost F actor, and repressors RegF and CrgA regulate transcription of pilE , the gene encoding the pilus structural subunit. The T ype IV pilus is also a strictly conserved trait in commensal N eisseria . We present evidence that a different mechanism regulates pilE transcription in commensals. Using N eisseria elongata as a model, we show that S igma factor RpoN (σ 54 ), I ntegration H ost F actor, and an activator we name N pa regulate pilE transcription. Taken in context with previous reports, our findings indicate pilE regulation switched from an RpoN ‐ to an RpoD ‐dependent mechanism as pathogenic N eisseria diverged from commensals during evolution. Our findings have implications for the timing of T fp expression and T fp‐mediated host cell interactions in these two groups of bacteria.