Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Differential disease resistance response in the barley necrotic mutant nec1 | Keisa et al. BMC Plant Biology 2011 11 66 http 1471-2229 11 66 BMC Plant Biology RESEARCH ARTICLE Open Access Differential disease resistance response in the barley necrotic mutant necl Anete Keisa Krista Kanberga-Silina Ilva Nakurte Laura Kunga and Nils Rostoks Abstract Background 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. Arabidopsis thaliana CNGC4 mutants hlml and dnd2 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 nec1 comprising of a frame-shift mutation of CNGC4 displays a necrotic phenotype and constitutively over-expresses PR-1 yet it is not known what effect the nec1 mutation has on barley resistance against different types of pathogens. Results nec1 mutant accumulated high amount of SA and hydrogen peroxide compared to parental cv. Parkland. Experiments investigating nec1 disease resistance demonstrated positive effect of nec1 mutation on non-host resistance against Pseudomonas syringae pv. tomato Pst at high inoculum density whereas at normal Pst inoculum concentration nec1 resistance did not differ from wt. In contrast to augmented P. syringae resistance penetration resistance against biotrophic fungus Blumeria graminis f. sp. hordei Bgh the causal agent of powdery mildew was not altered in nec1. The nec1 mutant significantly over-expressed race non-specific Bgh resistance-related genes BI-1 and MLO. Induction of BI-1 and MLO suggested putative involvement of nec1 in race non-specific Bgh resistance therefore the effect of nec1on mlo-5-mediated Bgh resistance was assessed. The nec1 mlo-5 double
