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. 2020 Feb 5;11:122. doi: 10.3389/fmicb.2020.00122

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Copyright © 2020 Meng, Huang, Huang, Liu, Han and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Working model of the relationship between OPGs and the Rcs phosphorelay in Y. enterocolitica. (A) In the wild-type strain, the Rcs system represses cell motility, division and biofilm formation by inhibiting flhDC, ftsAZ, and hmsHFRS expression. (B) OPGs deficiency activates the Rcs phosphorelay and inhibits flhDC, ftsAZ, and hmsHFRS expression, resulting in further repression of cell motility, division, and biofilm formation. (C–E) Disruption of the Rcs phosphorelay pathway downregulates RcsB phosphorylation, restoring cell motility, division, and biofilm formation by enhancing the expression of flhDC, ftsAZ, and hmsHFRS.