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. 2022 Oct 13;74(1):118–129. doi: 10.1093/jxb/erac403

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© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Experimental Biology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 7. — A model for the role of MON1 and the Blumeria hordei (Bh) effector CSEP0162 in immunity. MON1-activation of RabG associated with multivesicular bodies (MVB) contributes to immunity in several ways. (1) It allows the MVB to fuse with the plasma membrane (PM) for encasement formation. (2) It is required for coiled-coil nucleotide-binding leucine-rich repeat (CNL-)activated hypersensitive reaction (HR), as MVB fusion to the PM perhaps delivers a PM component required for CNL resistosome PM binding (2^a), or MVB fusion to the vacuole sends a CNL negative regulator for degradation. When this degradation is prevented, the CNL is inhibited (2^b). (3) In Arabidopsis, MON1 knockout leads to EDS1-dependent developmental defects. Thus, MON1 is predicted to be directly or indirectly monitored by a TNL, which at the same time is inhibited by MON1. Upon MON1 inactivation/removal, this TNL is activated to cause plant lesions. (4) CSEP0162 interacts with MON1 and small heat-shock proteins (sHSPs). This might induce a MON1/CSEP0162/sHSP complex, observed as an aggresome-like structure, whereby MON1 is prevented from functioning at the MVB.