Figure 1. PTI and ETI induce cytoplasmic Ca²⁺ elevations.

RKs and RPs are PRRs residing at the PM. They form complexes with co‐receptors upon perception of molecular patterns originating from microbes, viruses, herbivores, parasitic plants, or damaged host cells. In turn, RLCKs are activated and released from the complexes to activate downstream signaling to induce pattern‐triggered immunity, of which Ca²⁺ release within few minutes after ligand perception is one facet. Microbes introduce effector proteins into host cells to disturb and overcome immune responses. Cytoplasmic NLRs sense the presence or activity of effectors to induce ETI. To this end, autoinhibition is released, ADP is changed to ATP and oligomerization of NLRs occurs, leading to downstream signaling and finally ETI (A). A significant cytoplasmic Ca²⁺ increase has been reported to occur in Arabidopsis leaves starting 1.5 h and peaking at about 2 h after infection with avirulent bacteria (B). Schematic Ca²⁺ signatures of Arabidopsis plants induced by bacterial infection as reported by Grant et al (2000) (B). RK: receptor kinase; co‐RK: coreceptor kinase; RP: receptor protein; RLCK: receptor like cytoplasmic kinase; NLR: nucleotide‐binding leucine‐rich repeat receptor; CC: coiled‐coil; TIR: toll/interleukin‐related; CNLs: CC‐NLRs; TNLs: TIR‐NLRs; RNLs: RPW8‐NRLs; NBS: nucleotide binding site; LRR: leucine‐rich repeats; PTI: pattern‐triggered immunity; ETI: effector‐triggered immunity, c[Ca2^+]: cytoplasmic free Ca²⁺ concentration.