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Lacking an adaptive immune system, plants rely on innate immunity comprising two main layers: PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), both utilizing Ca 2+ influx and reactive oxygen species (ROS) for signaling. PTI, mediated by pattern-recognition receptors (PRRs), responds to conserved pathogen- or damage-associated molecular patterns. Some pathogens evade PTI using effectors, triggering plants to activate ETI. At the heart of ETI are nucleotide-binding leucine-rich repeat receptors (NLRs), which detect specific pathogen effectors and initiate a robust immune response. NLRs, equipped with a nucleotide-binding domain and leucine-rich repeats, drive a potent immune reaction starting with pronounced, prolonged cytosolic Ca 2+ influx, followed by increased ROS levels. This sequence of events triggers the hypersensitive response—a localized cell death designed to limit pathogen spread. This intricate use of Ca 2+ and ROS highlights the crucial role of NLRs in supplementing the absence of an adaptive immune system in plant innate immunity.
Weralupitiya et al. (2024) studied this question.