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Activation of the helper NRC4 immune receptor forms a hexameric resistosome

Affiliations
  • 1Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA, USA; Innovative Genomics Institute, University of California, Berkeley, Berkeley, CA, USA.
  • 2California Institute for Quantitative Biosciences (QB3), University of California, Berkeley, Berkeley, CA, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA, USA. Electronic address: zhenlinyang@berkeley.edu.
  • 3Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA, USA.
  • 4Innovative Genomics Institute, University of California, Berkeley, Berkeley, CA, USA.
  • 5Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.
  • 6Department of Molecular Biology, Princeton University, Princeton, NJ, USA.
  • 7Department of Biology and Howard Hughes Medical Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
  • 8Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA, USA; Innovative Genomics Institute, University of California, Berkeley, Berkeley, CA, USA. Electronic address: stask@berkeley.edu.

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August 2, 2024

Abstract

Innate immune responses to microbial pathogens are regulated by intracellular receptors known as nucleotide-binding leucine-rich repeat receptors (NLRs) in both the plant and animal kingdoms. Across plant innate immune systems, “helper” NLRs (hNLRs) work in coordination with “sensor” NLRs (sNLRs) to modulate disease resistance signaling pathways. Activation mechanisms of hNLRs based on structures are unknown. Our research reveals that the hNLR, known as NLR required for cell death 4 (NRC4), assembles into a hexameric resistosome upon activation by the sNLR Bs2 and the pathogenic effector AvrBs2. This conformational change triggers immune responses by facilitating the influx of calcium ions (Ca) into the cytosol. The activation mimic alleles of NRC2, NRC3, or NRC4 alone did not induce Ca influx and cell death in animal cells, suggesting that unknown plant-specific factors regulate NRCs’ activation in plants. These findings significantly advance our understanding of the regulatory mechanisms governing plant immune responses.

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