Intimate adhesion of Neisseria meningitidis to human epithelial cells is under the control of the crgA gene, a novel LysR-type transcriptional regulator

• Published in: The EMBO journal Vol. 19; no. 5; pp. 1068 - 1078
• Main Authors: Deghmane, Ala-Eddine, Petit, Stéphanie, Topilko, Andrzej, Pereira, Yannick, Giorgini, Dario, Larribe, Mireille, Taha, Muhamed-Kheir
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.03.2000; Blackwell Publishing Ltd; EMBO Press; Oxford University Press
• Subjects: Adhesion; Bacterial Adhesion; Bacterial Adhesion - genetics; Bacterial Proteins; Bacterial Proteins - genetics; Bacteriology; Base Sequence; Cell Line; crgA gene; CrgA protein; Epithelial Cells; Epithelial Cells - microbiology; Epithelial Cells - physiology; Gene Expression Regulation, Bacterial; Humans; intimate adhesion; Life Sciences; LysR protein; LysR-regulator; Meningococcal Infections; Meningococcal Infections - genetics; Meningococcal Infections - microbiology; Microbiology and Parasitology; Molecular Sequence Data; Neisseria meningitidis; Neisseria meningitidis - physiology; pilC1 gene; PilC1 protein; Transcription Factors; Transcription Factors - genetics; LysR-regulator; Neisseria meningitidis; intimate adhesion
• ISSN: 0261-4189; 1460-2075
• DOI: 10.1093/emboj/19.5.1068

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.