W076 Cell-wall based host-and nonhost resistance of barley against powdery mildew

Date: Saturday, January 14, 2012
Time: 2:50 PM
Room: San Diego
Dimitar Douchkov , Leibniz Inst. of Plant Genetics and Crop Plant Res., Gatersleben, Germany
Goetz Hensel , Leibniz Inst. of Plant Genetics & Crop Plant Research (IPK)
Jochen Kumlehn , Leibniz Inst. of Plant Genetics & Crop Plant Research (IPK)
Patrick Schweizer , Leibniz Inst. of Plant Genetics & Crop Plant Research (IPK), Gatersleben, Germany
Nonhost- as well as race-nonspecific host resistance are manifestations of pathogen-associated molecular pattern (PAMP)-triggered innate immunity of plants. Both are durable and therefore, of high interest to plant breeders. However, at least race-nonspecific host resistance are usually controlled by multiple quantitative trait loci and therefore, complicated to handle in breeding approaches. Knowing about the underlying genes would allow more targeted exploitation of the trait by allele introgressions or gene technology. In order to identify genes that mediate nonhost resistance of barley to the wheat powdery mildew fungus Blumeria graminis f.sp. tritici we performed an RNAi-based screening of 725 pathogen-upregulated transcripts (TIGS). This revealed 10 genes that caused partial breakdown of nonhost resistance upon TIGS. One of these encoded the pathogen-induced cellulase-synthase like protein HvCSLD2 suggesting a role in cell-wall de novo synthesis or re-shaping upon powdery mildew attack. Transgenic plants silenced in HvCSLD2 were supersusceptible to both the wheat- and barley powdery mildew and suffered from enhanced papilla penetration despite the accumulation of high amounts of callose and lignin-like materials. The transgenic phenotype could be rescued by a synthetic HvCSLD2 gene that was immune against the RNAi effect due to a high density of silent point mutations. Besides a deficit in disease resistance no pleiotrophic phenotype was observed in the RNAi lines. Therefore, HvCSLD2 is probably involved in locally induced cell-wall reshaping upon pathogen attack by a novel mechanism that is independent from the accumulation of callose and lignin-like materials.