The NAG Sensor NagC Regulates LEE Gene Expression and Contributes to Gut Colonization by Escherichia coli O157:H7. Guillaume Le Bihan, Jean-Félix Sicard, Philippe Garneau, et al. Front Cell Infect Microbiol. 2017 Apr 24;7:134. Speaker：Shu-Yu Liu(劉書羽) Time：15：10~16：00, Nov. 29,2017 Commentator：Dr. Ching-Hao Teng(鄧景浩) Place：Room 601 Abstract： Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is a human pathogen that can cause bloody diarrhea and renal failures. Type three secretion system (T3SS) is an important system for EHEC to attach directly to human intestinal epithelium and to form attaching and effacing (AE) lesions on host intestinal epithelial cells. The structure that forms AE lesion is encoded by the locus of enterocyte effacement (LEE). One of LEE genes encodes an LEE-activator Ler, which controlled by several regulators in response to intestinal metabolites such as mucin-derived sugar N-acetylglucosamine (NAG) and N-acetylneuraminic acid (NANA). NAG and NANA inhibit EHEC adhesion to epithelial cells through down-regulation of LEE expression. NagC is a sensor of NAG-6 phosphate (NAG-6P) which produced during the catabolism of NAG and NANA. NagC is also known as a DNA binding protein that can bind LEE1operon promoter to regulate LEE expression. Therefore, NagC is an important protein for LEE gene expression. By using mutant strains to demonstrate that NAG and NANA regulate LEE gene expression is NagC-depentend. Finally, the NAG-6P sensor NagC was confirmed to promote the adhesion of EHEC to intestinal cell in vitro through a direct regulation of ler and to be an important regulator for the fitness of EHEC in vivo. References: 1. Enteropathogenic and Enterohemorrhagic Escherichia coli Infections: Translocation, Translocation, Translocation. Infect Immun. 2005 May; 73(5): 2573–2585. CAP and Nag repressor binding to the regulatory regions of the nagE-B and manX genes of Escherichia coli. J Mol Biol. 1991 Feb 20;217(4):661-79.