4.5 Review

Life-or-death decisions in plant immunity

Journal

CURRENT OPINION IN IMMUNOLOGY
Volume 75, Issue -, Pages -

Publisher

CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2022.102169

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Funding

  1. National Institutes of Health [5R35-GM118036-06]
  2. National Science Foundation [IOS-2041378]
  3. Howard Hughes Medical Institute

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Upon pathogen challenge, plant cells defend themselves by triggering programmed cell death and secreting immune signals. Recent research has found that the oligomerization of immune receptors induced by pathogens acts as a switch for inhibitory proteins, resulting in the formation of a resistosome that triggers cell death. Synergy between different signaling pathways is necessary for sustained immune induction.
Upon pathogen challenge, plant cells can mount defense not only by triggering programmed cell death (PCD) to limit pathogen growth, but also by secreting immune signals to activate subsequent organism-scale defense responses. Recent advances in the study of plant immune mechanisms have found that pathogen-induced oligomerization of immune receptors is a common 'on' switch for the normally self-inhibitory proteins. The resulting `resistosome' triggers PCD through the formation of a calcium channel or a NADase. Synergy between different receptor-mediated signaling pathways appears to be required for sustained immune induction to trigger PCD of infected cells. In the neighboring cells, PCD is inhibited through the production of immune signal salicylic acid (SA) which mediates degradation of PCD-inducing immune components in biomolecular condensates. Future work is required to connect the resistosome-mediated channel formation and the NADase activity to the downstream regulation of immune execution.

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