Abstract
Plants are exposed to numerous pathogens and fend off many of these with different phytohormone signalling pathways. Much is known about defence signalling in the dicotyledonous model plant Arabidopsisthaliana, but it is unclear to which extent knowledge from model systems can be transferred to monocotyledonous plants, including cereal crops. Here, we investigated the defence-inducing potential of Arabidopsis resistance-inducing compounds in the cereal crop barley. Salicylic acid (SA), folic acid (Fol), and azelaic acid (AzA), each inducing defence against (hemi-)biotrophic pathogens in Arabidopsis, were applied to barley leaves and the treated and systemic leaves were subsequently inoculated with Xanthomonastranslucens pv. cerealis (Xtc), Blumeria graminis f. sp. hordei (powdery mildew, Bgh), or Pyrenophora teres. Fol and SA reduced Bgh propagation locally and/or systemically, whereas Fol enhanced Xtc growth in barley. AzA reduced Bgh propagation systemically and enhanced Xtc growth locally. Neither SA, Fol, nor AzA influenced lesion sizes caused by the necrotrophic fungus P. teres, suggesting that the tested compounds exclusively affected growth of (hemi-)biotrophic pathogens in barley. In addition to SA, Fol and AzA might thus act as resistance-inducing compounds in barley against Bgh, although adverse effects on the growth of pathogenic bacteria, such as Xtc, are possible.
Highlights
Plants are constantly challenged with a plethora of pathogens, including herbivorous insects, fungi, oomycetes, bacteria and viruses [1]
We report on the role of salicylic acid (SA), folic acid (Fol), and azelaic acid (AzA) on barley defence against pathogens with different lifestyles
We investigated the role of resistance-inducing compounds from Arabidopsis, salicylic acid (SA), folic acid, and azelaic acid, on barley defence against the pathogens Xanthomonas translucens, Blumeria graminis f. sp. hordei (Bgh), and Pyrenophora teres
Summary
Plants are constantly challenged with a plethora of pathogens, including herbivorous insects, fungi, oomycetes, bacteria and viruses [1] To cope with these attacks, plants have evolved an effective immune system of pre-formed and inducible defence mechanisms. After the first contact between plant and pathogen, conserved structures such as bacterial flagellin or fungal chitin—so-called pathogen-associated molecular patterns (PAMPs)—encounter pattern recognition receptors on the cell surface. This triggers a first immune response termed PAMP-triggered immunity (PTI) [2,4,5]. In response to this development, plants evolved resistance (R) genes, which encode proteins that directly or indirectly recognise effectors, and on recognition elicit so called effector-triggered immunity (ETI) [2,3,4,6]
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