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Expression of the meningococcal adhesin NadA is controlled by a transcriptional regulator of the MarR family
Author(s) -
Schielke Stephanie,
Huebner Claudia,
Spatz Carolin,
Nägele Virginie,
Ackermann Nikolaus,
Frosch Matthias,
Kurzai Oliver,
SchubertUnkmeir Alexandra
Publication year - 2009
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/j.1365-2958.2009.06710.x
Subject(s) - biology , bacterial adhesin , neisseria meningitidis , neisseria gonorrhoeae , virulence , mutant , gene , microbiology and biotechnology , genetics , pathogen , adaptation (eye) , neisseria , biogenesis , bacteria , neuroscience
Summary Two closely related pathogenic species have evolved in the genus Neisseria : N. meningitidis and N. gonorrhoeae , which occupy different host niches and cause different clinical entities. In contrast to the pathogen N. gonorrhoeae , N. meningitidis is a commensal and only rarely becomes invasive. Little is known about the genetic background of the entirely different lifestyles in these closely related species. Meningococcal NMB1843 encodes a transcriptional regulator of the MarR family. The gonococcal homologue FarR regulates expression of farAB , mediating fatty acid resistance. We show that Nm FarR also directly interacts with NmfarAB . Yet, by contrast to N. gonorrhoeae , no significant sensitivity to fatty acids was observed in a Δ farR mutant due to intrinsic resistance of meningococci. Further analyses identified an Nm FarR‐repressed protein absent from N. gonorrhoeae . This protein is the meningococcus‐specific adhesin and vaccine component NadA that has most likely been acquired by horizontal gene transfer. Nm FarR binds to a 16 base pair palindromic repeat within the nadA promoter. De‐repression of nadA resulted in significantly higher association of a Δ farR strain with epithelial cells. Hence Nm FarR has gained control over a meningococcus‐specific gene involved in host colonization and thus contributed to divergent niche adaptation in pathogenic Neisseriae .