Negative control in two-component signal transduction by transmitter phosphatase activity
Article first published online: 29 SEP 2011
© 2011 Blackwell Publishing Ltd
Volume 82, Issue 2, pages 275–286, October 2011
How to Cite
Huynh, T. N. and Stewart, V. (2011), Negative control in two-component signal transduction by transmitter phosphatase activity. Molecular Microbiology, 82: 275–286. doi: 10.1111/j.1365-2958.2011.07829.x
- Issue published online: 12 OCT 2011
- Article first published online: 29 SEP 2011
- Accepted manuscript online: 6 SEP 2011 09:56AM EST
- Accepted 30 August, 2011.
Bifunctional sensor transmitter modules of two-component systems exert both positive and negative control on the receiver domain of the cognate response regulator. In negative control, the transmitter module accelerates the rate of phospho-receiver dephosphorylation. This transmitter phosphatase reaction serves the important physiological functions of resetting response regulator phosphorylation level and suppressing cross-talk. Although the biochemical reactions underlying positive control are reasonably well understood, the mechanism for transmitter phosphatase activity has been unknown. A recent hypothesis is that the transmitter phosphatase reaction is catalysed by a conserved Gln, Asn or Thr residue, via a hydrogen bond between the amide or hydroxyl group and the nucleophilic water molecule in acyl-phosphate hydrolysis. This hypothetical mechanism closely resembles the established mechanisms of auxiliary phosphatases such as CheZ and CheX, and may be widely conserved in two-component signal transduction. In addition to the proposed catalytic residues, transmitter phosphatase activity also requires the correct transmitter conformation and appropriate interactions with the receiver. Evidence suggests that the phosphatase-competent and autokinase-competent states are mutually exclusive, and the corresponding negative and positive activities are likely to be reciprocally regulated through dynamic control of transmitter conformations.