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Intimate adhesion of Neisseria meningitidis to human epithelial cells is under the control of the crgA gene, a novel LysR‐type transcriptional regulator
Author(s) -
Deghmane AlaEddine,
Petit Stéphanie,
Topilko Andrzej,
Pereira Yannick,
Giorgini Dario,
Larribe Mireille,
Taha MuhamedKheir
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.5.1068
Subject(s) - biology , gene , transcriptional regulation , promoter , mutant , microbiology and biotechnology , pilus , regulator , regulation of gene expression , gene expression , genetics , virulence
PilC1, a pilus‐associated protein in Neisseria meningitidis , is a key element in initial meningococcal adhesion to target cells. A promoter element (CREN, contact regulatory element of Neisseria ) is responsible for the transient induction of this gene upon cell contact. crgA (contact‐regulated gene A) encodes a transcriptional regulator whose expression is also induced upon cell contact from a promoter region similar to the CREN of pilC1 . CrgA shows significant sequence homologies to LysR‐type transcriptional regulators. Its inactivation in meningococci provokes a dramatic reduction in bacterial adhesion to epithelial cells. Moreover, this mutant is unable to undergo intimate adhesion to epithelial cells or to provoke effacing of microvilli on infected cells. Purified CrgA is able to bind to pilC1 and crgA promoters, and CrgA seems to repress the expression of pilC1 and crgA . Our results support a dynamic model of bacteria–cell interaction involving a network of regulators acting in cascade. CrgA could be an intermediate regulator in such a network.

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