Shared signals, different fates: Calcium and ROS in plant PRR and NLR immunity.

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 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 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 and ROS highlights the crucial role of NLRs in supplementing the absence of an adaptive immune system in plant innate immunity.