Soil salinization is a major threat to agriculture in arid and semi-arid regions, where water scarcity and inadequate drainage of irrigated lands severely reduce crop yield. Salt accumulation inhibits plant growth and reduces the ability to uptake water and nutrients, leading to osmotic or water-deficit stress. Salt is also causing injury of the young photosynthetic leaves and acceleration of their senescence, as the Na+ cation is toxic when accumulating in cell cytosol resulting in ionic imbalance and toxicity of transpiring leaves. To cope with salt stress, plants have evolved mainly two types of tolerance mechanisms based on either limiting the entry of salt by the roots, or controlling its concentration and distribution. Understanding the overall control of Na+ accumulation and functional studies of genes involved in transport processes, will provide a new opportunity to improve the salinity tolerance of plants relevant to food security in arid regions. A better understanding of these tolerance mechanisms can be used to breed crops with improved yield performance under salinity stress. Moreover, associations of cultures with nitrogen-fixing bacteria and arbuscular mycorrhizal fungi could serve as an alternative and sustainable strategy to increase crop yields in salt-affected fields.

To investigate the resistance signaling pathways activated by pathogen infection, we previously identified the Arabidopsis thaliana mutant constitutive expresser of PR genes22 (cpr22), which displays constitutive activation of multiple defense responses. Here, we identify the cpr22 mutation as a 3-kb deletion that fuses two cyclic nucleotide-gated ion channel (ATCNGC)-encoding genes, ATCNGC11 and ATCNGC12, to generate a novel chimeric gene, ATCNGC11/12. Genetic, molecular, and complementation analyses suggest that ATCNGC11/12, as well as ATCNGC11 and ATCNGC12, form functional cAMP-activated ATCNGCs and that the phenotype conferred by cpr22 is attributable to the expression of ATCNGC11/12. However, because overexpression of ATCNGC12, but not ATCNGC11, suppressed the phenotype conferred by cpr22, the development of this phenotype appears to be regulated by the ratio between ATCNGC11/12 and ATCNGC12. Analysis of knockout lines revealed that both ATCNGC11 and ATCNGC12 are positive mediators of resistance against an avirulent biotype of Hyaloperonospora parasitica. Through epistatic analyses, cpr22-mediated enhanced resistance to pathogens was found to require NDR1-dependent and EDS1/PAD4-dependent pathways. In striking contrast, none of these pathways was required for cpr22-induced salicylic acid accumulation or PR-1 gene expression. These results demonstrate that NDR1, EDS1, and PAD4 mediate other resistance signaling function(s) in addition to salicylic acid and pathogenesis-related protein accumulation. Moreover, the requirement for both NDR1-dependent and EDS1/PAD4-dependent pathways for cpr22-mediated resistance suggests that these pathways are cross-regulated.

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