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Death Don't Have No Mercy and Neither Does Calcium: Arabidopsis CYCLIC NUCLEOTIDE GATED CHANNEL2 and Innate Immunity^[W]

Agricultural Biotechnology Laboratory, University of Connecticut, Storrs, Connecticut 06269-4163

¹ To whom correspondence should be addressed. E-mail gerald.berkowitz{at}uconn.edu; fax 860-486-0534.

Plant innate immune response to pathogen infection includes an elegant signaling pathway leading to reactive oxygen species generation and resulting hypersensitive response (HR); localized programmed cell death in tissue surrounding the initial infection site limits pathogen spread. A veritable symphony of cytosolic signaling molecules (including Ca²⁺, nitric oxide [NO], cyclic nucleotides, and calmodulin) have been suggested as early components of HR signaling. However, specific interactions among these cytosolic secondary messengers and their roles in the signal cascade are still unclear. Here, we report some aspects of how plants translate perception of a pathogen into a signal cascade leading to an innate immune response. We show that Arabidopsis thaliana CYCLIC NUCLEOTIDE GATED CHANNEL2 (CNGC2/DND1) conducts Ca²⁺ into cells and provide a model linking this Ca²⁺ current to downstream NO production. NO is a critical signaling molecule invoking plant innate immune response to pathogens. Plants without functional CNGC2 lack this cell membrane Ca²⁺ current and do not display HR; providing the mutant with NO complements this phenotype. The bacterial pathogen–associated molecular pattern elicitor lipopolysaccharide activates a CNGC Ca²⁺ current, which may be linked to NO generation due to buildup of cytosolic Ca²⁺/calmodulin.

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