Mechanism of chemotaxis in E Mechanism of chemotaxis in E. coli and role of the PTS in carbohydrate chemotaxis. Mechanism of chemotaxis in E. coli and role of the PTS in carbohydrate chemotaxis. In the absence of chemotactically active molecules (top left), CheA autophosphorylates at a histidyl residue. This reaction is stimulated by CheW, which recruits CheA to the MCP receptor protein. P∼CheA transfers its phosphoryl group to CheY, and P∼CheY binds the flagellar motor FliM, thereby evoking clockwise (CW) rotation of the flagella, which leads to tumbling of the bacterium. In the presence of chemotactically active molecules (top right), the autophosphorylation activity of CheA is inhibited, and as a result, the concentration of P∼CheY drops. FliM molecules will no longer be complexed with CheY, which favors counterclockwise (CCW) rotation of the flagella. This results in smooth swimming towards increasing concentrations of the chemotactically active substance. The presence of an efficiently metabolizable PTS carbohydrate (or the absence of PEP) induces a similar response, as under these conditions, EI is present mainly in an unphosphorylated form. In fact, dephospho-EI inhibits the autophosphorylation of CheA (center) and therefore also favors smooth swimming. The sensitivity of the system towards the signal is regulated through methylation and demethylation of the MCPs (bottom), which are catalyzed by CheR and CheB, respectively. MCP methylation stimulates the autophosphorylation of CheA, and demethylation inhibits it. Josef Deutscher et al. Microbiol. Mol. Biol. Rev. 2006; doi:10.1128/MMBR.00024-06