<p>Abstract</p> <p>Background</p> <p>Although ion fluxes are considered to be an integral part of signal transduction during responses to pathogens, only a few ion channels are known to participate in the plant response to infection. CNGC4 is a disease resistance-related cyclic nucleotide-gated ion channel. <it>Arabidopsis thaliana </it>CNGC4 mutants <it>hlm1 </it>and <it>dnd2 </it>display an impaired hypersensitive response (HR), retarded growth, a constitutively active salicylic acid (SA)-mediated pathogenesis-related response and elevated resistance against bacterial pathogens. Barley CNGC4 shares 67% aa identity with AtCNGC4. The barley mutant <it>nec1 </it>comprising of a frame-shift mutation of CNGC4 displays a necrotic phenotype and constitutively over-expresses <it>PR-1</it>, yet it is not known what effect the <it>nec1 </it>mutation has on barley resistance against different types of pathogens.</p> <p>Results</p> <p><it>nec1 </it>mutant accumulated high amount of SA and hydrogen peroxide compared to parental cv. Parkland. Experiments investigating <it>nec1 </it>disease resistance demonstrated positive effect of <it>nec1 </it>mutation on non-host resistance against <it>Pseudomonas syringae </it>pv. <it>tomato </it>(<it>Pst</it>) at high inoculum density, whereas at normal <it>Pst </it>inoculum concentration <it>nec1 </it>resistance did not differ from wt. In contrast to augmented <it>P. syringae </it>resistance, penetration resistance against biotrophic fungus <it>Blumeria graminis </it>f. sp. <it>hordei </it>(<it>Bgh</it>), the causal agent of powdery mildew, was not altered in <it>nec1</it>. The <it>nec1 </it>mutant significantly over-expressed race non-specific <it>Bgh </it>resistance-related genes <it>BI-1 </it>and <it>MLO</it>. Induction of <it>BI-1 </it>and <it>MLO </it>suggested putative involvement of <it>nec1 </it>in race non-specific <it>Bgh </it>resistance, therefore the effect of <it>nec1</it>on <it>mlo-5</it>-mediated <it>Bgh </it>resistance was assessed. The <it>nec1</it>/<it>mlo-5 </it>double mutant was as resistant to <it>Bgh </it>as <it>Nec1</it>/<it>mlo-5 </it>plants, suggesting that <it>nec1 </it>did not impair <it>mlo-5 </it>race non-specific <it>Bgh </it>resistance.</p> <p>Conclusions</p> <p>Together, the results suggest that <it>nec1 </it>mutation alters activation of systemic acquired resistance-related physiological markers and non-host resistance in barley, while not changing rapid localized response during compatible interaction with host pathogen. Increased resistance of <it>nec1 </it>against non-host pathogen <it>Pst </it>suggests that <it>nec1 </it>mutation may affect certain aspects of barley disease resistance, while it remains to be determined, if the effect on disease resistance is a direct response to changes in SA signaling.</p
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