Resistance in barley against the powdery mildew fungus ( Erysiphe graminis | f.sp. hordei | ) is not associated with enhanced levels of endogenous jasmonates
Onset of acquired resistance of barley ( Hordeum vulgare) chemically induced by 2,6-dichloroisonicotinic acid (DCINA) correlated with the accumulation of mRNA homologous to cDNA pHvJ256 which codes for a soluble leaf-thionin with a Mr. of 6 kDa [Wasternack et al., 1994a]. In the present work, we ext...
|Published in:||European Journal of Plant Pathology : Published in cooperation with the European Foundation for Plant Pathology, Vol. 101, No. 3 (1995), p. 319-332|
|Other Involved Persons:||; ; ; ;|
|QR Code:||Show QR Code|
- Onset of acquired resistance of barley ( Hordeum vulgare) chemically induced by 2,6-dichloroisonicotinic acid (DCINA) correlated with the accumulation of mRNA homologous to cDNA pHvJ256 which codes for a soluble leaf-thionin with a Mr. of 6 kDa [Wasternack et al., 1994a]. In the present work, we extend this finding by showing that the thionin transcript also accumulated following treatment of barley with the resistance-inducing compounds 3,5-dichlorosalicylic acid (DCSA), salicylic acid (SA), and an extract from Bacillus subtilis. The polypeptide showed antifungal activity against the biotrophic cereal pathogens Erysiphe graminis f.sp. hordei and Puccinia graminis f.sp. tritici which may indicate a possible role in the mechanism of acquired resistance in barley. A thionin transcript hybridizing to pHvJ256 accumulated also in response to application of jasmonates, or treatments that elevated endogenous amounts of the plant growth substance, pointing to the possibility that signaling mediating defense responses in barley involves jasmonates. However, a topical spray application of jasmonic acid (JA) or jasmonate methyl ester (JM) did not protect barley leaves against infection by E. graminis. Performing a kinetic analysis by an enzyme immunoassay specific for (−)-JA, (−)-JM, and its amino acid conjugates, accumulation of jasmonates was detected in osmotically stressed barley but not at the onset of chemically induced or genetically based resistance governed by the powdery mildew resistance genes Mlg, Mla12, or mlo5. Furthermore, the jasmonate-inducible proteins JIP-23 and JIP-60 were strongly induced following JM- but not DCINA-treatment or inoculation with E. graminis. Hence, in barley, no indications were found in favour for the previously proposed model of a lipid-based signaling pathway via jasmonates mediating expression of resistance in plants against pathogens.