Cyclic nucleotide-gated ion channel-mediated cell death may not be critical for R gene-conferred resistance to Cucumber mosaic virus in Arabidopsis thaliana

Virus multiplication is dependent on host metabolism. Thus, cell death at the primary site of virus infection seems to be critical for defense against virus infection. However, the importance of cell death in hypersensitive response (HR) resistance against viruses in host plants is still unclear. To investigate the role of cell death in virus resistance, we analyzed the response of the Arabidopsis defense, no death (dnd) mutant to Cucumber mosaic virus (CMV) in the presence of RCY1 encoding a CC-NB-LRR class R-protein in the background of ecotype Col-0. The dnd1 phenotype, loss of HR cell death without loss of gene-for-gene resistance to bacterial pathogens, is caused by mutation of the gene encoding the cyclic nucleotide-gated ion channel AtCNGC2. In virus-inoculated leaves of the dnd1 mutant carrying RCY1 (RCY1 dnd1), the induction of HR cell death at the site of virus infection was significantly compromised. However, like wild-type carrying RCY1, local and systemic spread of the virus was restricted and expression of pathogenesis-related (PR) genes was induced in the RCY1 dnd1 mutant. The response to CMV in the RCY1 dnd1 mutant, which was transformed with a salicylic acid-inducible promoter P4::green fluorescence protein-coding region (P4pro::GFP) construct, suggested that the salicylic acid signaling pathway was activated at the site of virus infection without induction of HR cell death. Thus, DND1-mediated HR cell death may not play a critical role in RCY1-conferred resistance to CMV in Arabidopsis.

► RCY1-mediated HR cell death in response to CMV was compromised by dnd1 mutation.
► In plants carrying dnd1 and RCY1, virus multiplication and spread were restricted.
► DND1-mediated HR cell death may not be required for RCY1-conferred resistance to CMV.