TheArabidopsis dnd1“defense, no death” gene encodes a mutated cyclic nucleotide-gated ion channel

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Abstract
Gene-for-gene disease resistance typically includes a programmed cell death response known as the hypersensitive response (HR). TheArabidopsis thaliana dnd1mutant was previously isolated as a line that failed to produce the HR in response to avirulentPseudomonas syringaepathogens; plants homozygous for the recessivednd1-1mutation still carry out effective gene-for-gene resistance. Thednd1-1mutation also causes constitutive systemic resistance and elevated levels of salicylic acid. In the present study, a positional cloning approach was used to isolateDND1. DND1encodes the same protein as AtCNGC2, a cyclic nucleotide-gated ion channel of previously unknown organismal function that can allow passage of Ca2+, K+and other cations [Leng, Q., Mercier, R. W., Yao, W. & Berkowitz, G. A. (1999)Plant Physiol.121, 753–761]. By using a nahG transgene, we found that salicylic acid is required for the elevated resistance caused by thednd1mutation but that removal of salicylic acid did not completely eliminate the dwarf and loss-of-HR phenotypes of mutantdnd1plants. A stop codon that would severely truncate theDND1gene product was identified in thednd1-1allele. This demonstrates that broad-spectrum disease resistance and inhibition of the HR can be activated in plants by disruption of a cyclic nucleotide-gated ion channel.