Abstract
The cytosolic signaling molecules Ca, nitric oxide (NO), cyclic nucleotides (cNMP), and calmodulin (CaM) are early components of the plant pathogen hypersensitive response (HR) signaling pathway. Interactions amongst these molecules and delineation of their roles in the signal cascade are unclear. We identify the first ion channel gene product, the cNMP gated channel (CNGC) AtCNGC2, associated with Ca influx into the plant cell and show how this influx leads to NO production. NO is a critical signaling molecule invoking plant innate immune response to pathogens. We find that lack of HR in loss-of-function Atcngc2 mutant plants is due to a block in NO generation. Patch clamp recordings of guard cell plasma membranes demonstrated that the bacterial elicitor lipopolysaccharide activates a CNGC Ca current. Monitoring of NO generation in leaf guard cells indicated that pathogen-induced Ca current is linked to NO generation due to build up of cytosolic Ca/CaM; Ca/CaM buildup also inactivates AtCNGC2. The interplay of cytosolic secondary messengers allows for generation of the cellular Ca spike involved in this signaling pathway. A model will be presented detailing these newly identified steps in plant innate immunity signaling.