The signal for adaptation

Accordingly, the sequence of events appears to be as follows Negative stimulation results in enhanced autophosphorylation of CheA, which, in turn, increases the steady-state phosphorylation level of CheY and, more slowly, of CheB. The increased phosphorylation level of CheY results in increased probability of clockwise rotation. As CheB becomes phosphorylated it is activated, the methylation level of the proper MCP is reduced, and the probability of clockwise rotation decreases to the prestimulus level. Conversely, positive stimulation 

Several observations, made in the nineteen eighties, that strains deleted for both cheR and cheB can partially adapt ([700, 701, 705, 772] and references therein), suggested that methylation and demethylation might 

A common denominator for the methylation-dependent adaptation and the CheZ-dependent termination or adaptation is that both processes are triggered by changes in the phosphorylation level of CheY. It appears that the complete mechanism of adaptation, methylation-dependent and independent, is still not fully resolved. Methylation-independent adaptation was also demonstrated in B. subtilis, where it was found to be very effective [366]. 

It has been known for some time that some two-component regulatory systems of E. coli (e.g., PhoR/PhoB [415, 762], NtrB/NtrC [226], and EnvZ/OmpR [230, 231, 488]) can function even in the absence of their histidine kinase. Each of these systems may possibly undergo crossregulation with another signal transduction system or it may possess an additional (yet-unidentified) signal transduction pathway [763]. Barak and Eisenbach [59] were surprised to realize that such a phenomenon 

Variations in signal transduction pathways in other bacterial species 

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