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. 2019 Jan 8;165(2):146–162. doi: 10.1099/mic.0.000758

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© 2019 The Authors

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 7. — An alternative model for PdhS2 regulation of CtrA activity. Our data are consistent with PdhS2 intersecting the DivK–CtrA regulatory pathway at one of two points. Pathway A: canonical genetic model with PdhS2 interacting with DivK. The phosphorylation status of DivK then modulates CtrA activity through the CckA–ChpT–CtrA axis. Pathway B: DivK-independent model of CtrA regulation by PdhS2 through an unidentified response regulator, RR-X. Both routes to the regulation of CtrA activity ultimately affect the phosphorylation status of CtrA, affecting occupancy at CtrA-regulated promoters, and finally leading to inverse regulation of attachment (primarily through cdGMP pools) and separately motility. Regulatory proteins: blue text; histidine kinases; orange text, histidine phosphotransferase (Hpt), green text, response regulators. RR-X indicates a putative response regulator, yet to be identified.