Enterohaemorrhagic Escherichia coli O157:H7 causes a characteristic histopathology in intestinal cells known as attaching and effacing lesion. The genes for the lesion are encoded by the Locus of Enterocyte Effacement (LEE) pathogenicity island, that encodes a type III secretion system, the intimin intestinal colonization factor, and the translocated intimin receptor protein that is translocated from the bacterium to the host epithelial cells. Expression of the operons encoded within LEE is complex, but recent studies have demonstrated that quorum sensing influences transcription from four of the LEE operon promoters. A transcriptional regulator (LuxR homologue), signal synthase (LuxI homologue), and autoinducer (acylhomoserine lactone) are indispensable for this system in most gram-negative bacteria. Vibrio harveyi, a gram-negative bioluminescent marine bacterium, regulates light production in response to two autoinducers (AI-1 and AI-2). AI-1 is a homoserine lactone produced by most gram-negative bacteria. The structure of AI-2 is not known, but many species of gram positive and gram-negative bacteria, including E. coli and more specifically O157:H7, have been shown to produce AI-2 depending on the function encoded by the luxS gene. The LuxS acts as an AI-2 synthase and the AI-2 is produced from S-adenosylmethionine in three enzymatic steps. The substrate for LuxS is S-ribosylhomocysteine, which is cleaved to form two products, one of which is homocysteine, and the other is AI-2. The biosynthetic pathways and the biochemical intermediates in AI-2 biosynthesis have been observed to be identical in several gram-negative bacteria, such as E. coli, Salmonella typhimurium, V. harveyi, Vibrio cholerae, and Enterococcus faecalis. Thus, unlike quorum sensing via the family of related homoserine autoinducers, AI-2 is a universal signal, which may be used by a variety of bacteria for communication among and between species and may be responsible for regulation of virulence genes in E. coli O157:H7.