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. Author manuscript; available in PMC: 2010 Mar 9.
Published in final edited form as: Mol Plant Pathol. 2009 Nov;10(6):777–793. doi: 10.1111/j.1364-3703.2009.00586.x

Fig. 2.

Fig. 2

AvrPtoB virulence activity in Arabidopsis. (A) In the absence of AvrPtoB, FLS2 and CERK1 recognize flagellin and an unknown molecule as pathogen (or microbe)-associated molecular patterns (PAMPs), respectively, leading to PAMP-triggered immunity (PTI). (B) Delivery of the N-terminal region of AvrPtoB suppresses the induction of PTI by flagellin by disrupting the FLS2–BAK1 complex necessary for signalling and by possibly inhibiting FLS2 and CERK1 kinase activity. (C) Delivery of full-length AvrPtoB suppresses PTI in the same manner as the N-terminal region. In addition, the C-terminal E3 ubiquitin ligase domain may promote ubiquitination of FLS2 and CERK1, either directly or by the endogenous receptor recycling pathway that functions through the 26S proteasome or the vacuolar degradation pathways. Degradation of the activated receptors may provide insurance that the receptor remains inactive after AvrPtoB dissociates and frees up the effector to act on another substrate.