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

Cian Duggan, Eleonora Moratto, Zachary Savage, Eranthika Hamilton, Hiroaki Adachi, Chih-Hang Wu, Alexandre Y. Leary, Yasin Tumtas, Stephen M. Rothery, Abbas Maqbool, Seda Nohut, Toby Ross Martin, Sophien Kamoun, Tolga Osman Bozkurt

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

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.
Original languageEnglish
Article numbere2104997118
JournalProceedings of the National Academy of Sciences of the United States of America (PNAS)
Volume118
Issue number34
Early online date20 Aug 2021
DOIs
Publication statusPublished - 24 Aug 2021

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