In Escherichia coli, chemotaxis feedback regulation couples receptor activity to modification of the receptors by CheR and CheB. It is a molecular example of negative feedback supporting signaling adaptation, with precision and kinetics assessed by the chemotaxis FRET assay above.
Removal of methyl groups from a modified receptor. In chemotaxis feedback regulation, this reverses the chemical modification introduced by receptor methylation; the two processes have different enzyme-dependent rates. Whether the demethylation rate depends on total receptor modification or on active receptors matters for perfect adaptation.
A conceptual chemotaxis adaptation model in which saturated CheR action supplies receptor methylation while CheB preferentially demethylates active receptors. If , the steady state output is , independent of ligand whenever a physically accessible stable steady state exists. Changing enzyme abundance can change this baseline without destroying adaptation to a subsequent ligand step.[ref]
If the forward receptor-modification flux depends on remaining unmethylated substrate, it generally depends indirectly on ligand through the modified receptor pool. The steady output then need not be ligand independent. Near-perfect adaptation may remain in a saturation limit; finite modification capacity and completely inactive receptor populations also bound the ideal perfect-adaptation result.
Return of an output to its original steady value after a persistent input change, with the adaptation property persisting over a range of model parameters. integral action can implement this property under stability and operating-range assumptions.
CheW is a coupling protein linking chemotaxis receptor arrays to CheA-associated signalling complexes. Removing it from a reconstituted system can test its functional requirement, while a physical-interface assay addresses direct contacts.
CheA is the signaling enzyme that promotes phosphorylation of CheY and CheB in the chemotaxis feedback regulation pathway.
CheB is an enzyme that reverses receptor methylation in chemotaxis; its regulation contributes to negative feedback.
CheR is an enzyme that catalyzes receptor methylation in chemotaxis, contributing to signaling adaptation.
The phosphorylation state of the protein CheY connects receptor signaling to motor behavior in Escherichia coli.
The chemotaxis FRET assay uses Förster resonance energy transfer between fluorescent tags on CheY and CheZ to report their association. Interpreting this emission ratio as CheA activity requires the coupling between CheY phosphorylation and CheZ binding described in the experimental sources above.
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