Dynamic localization of a helper NLR at the plant–pathogen interface underpins pathogen recognition

Duggan, Cian, Moratto, Eleonora, Savage, Zachary, Hamilton, Eranthika, Adachi, Hiroaki, Wu, Chih-Hang, Leary, Alexandre Y., Tumtas, Yasin, Rothery, Stephen M., Maqbool, Abbas, Nohut, Seda, Martin, Toby Ross, Kamoun, Sophien ORCID: https://orcid.org/0000-0002-0290-0315 and Bozkurt, Tolga Osman (2021) Dynamic localization of a helper NLR at the plant–pathogen interface underpins pathogen recognition. Proceedings of the National Academy of Sciences of the United States of America (PNAS), 118 (34). ISSN 0027-8424

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Abstract

Plants employ sensor–helper pairs of NLR immune receptors to recognize pathogen effectors and activate immune responses. Yet, the subcellular localization of NLRs pre- and postactivation during pathogen infection remains poorly understood. Here, we show that NRC4, from the “NRC” solanaceous helper NLR family, undergoes dynamic changes in subcellular localization by shuttling to and from the plant–pathogen haustorium interface established during infection by the Irish potato famine pathogen Phytophthora infestans. Specifically, prior to activation, NRC4 accumulates at the extrahaustorial membrane (EHM), presumably to mediate response to perihaustorial effectors that are recognized by NRC4-dependent sensor NLRs. However, not all NLRs accumulate at the EHM, as the closely related helper NRC2 and the distantly related ZAR1 did not accumulate at the EHM. NRC4 required an intact N-terminal coiled-coil domain to accumulate at the EHM, whereas the functionally conserved MADA motif implicated in cell death activation and membrane insertion was dispensable for this process. Strikingly, a constitutively autoactive NRC4 mutant did not accumulate at the EHM and showed punctate distribution that mainly associated with the plasma membrane, suggesting that postactivation, NRC4 may undergo a conformation switch to form clusters that do not preferentially associate with the EHM. When NRC4 is activated by a sensor NLR during infection, however, NRC4 forms puncta mainly at the EHM and, to a lesser extent, at the plasma membrane. We conclude that following activation at the EHM, NRC4 may spread to other cellular membranes from its primary site of activation to trigger immune responses.

Item Type: Article
Additional Information: Author acknowledgements: We thank Dr. Sebastian Schornack, Dr. Khaoula Belhaj, and Dr. Yasin Dagdas for the great comments and suggestions over the years. We thank Dr. Joe Win for sending materials and for the discussions. We thank the following funding agencies: Imperial Schrödinger PhD Scholarship (C.D.), Research England UK GCRF (C.D.), BBSRC (Grant BB/T006102/1) (C.D.), BBSRC DTP (E.M., Z.S., and A.Y.L.), and Gatsby Charitable Foundation (H.A., C.-H.W., A.M., and S.K.). The Facility for Imaging by Light Microscopy (S.M.R.) at Imperial College London is partly supported by funding from the Wellcome Trust (Grant 104931/Z/14/Z) and BBSRC (Grant BB/L015129/1).
Uncontrolled Keywords: cell biology,helper nlr,host–microbe interactions,plant disease resistance,general ,/dk/atira/pure/subjectarea/asjc/1000
Faculty \ School:
Faculty of Science > School of Biological Sciences
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Depositing User: LivePure Connector
Date Deposited: 18 Nov 2021 01:53
Last Modified: 30 Oct 2022 00:56
URI: https://ueaeprints.uea.ac.uk/id/eprint/82156
DOI: 10.1073/pnas.2104997118

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