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Molecular Characterization of Two Types of Resistance in Sunflower to Plasmopara halstedii, the Causal Agent of Downy Mildew

First author: National Soybean Research Center, 1101 W. Peabody Drive, University of Illinois at Urbana-Champaign, Urbana 61801; and second and third authors: UMR 1095 INRA-UBP, GDEC Génétique Diversité Ecophysiologie des Céréales, Université Blaise Pascal, 24 avenue des Landais 63177 Aubière Cedex, France.

Depending on host–pathotype combination, two types of sunflower–Plasmopara halstedii incompatibility reactions have previously been identified. Type I resistance can restrict the growth of the pathogen in the basal region of the hypocotyls, whereas type II cannot, thus allowing the pathogen to reach the cotyledons. In type II resistance, a large portion of the hypocotyls is invaded by the pathogen and, subsequently, a hypersensitive reaction (HR) is activated over a long portion of the hypocotyls. Thus, the HR in type II resistance coincides with a higher induction of hsr203j sunflower homologue in comparison with type I resistance, where the HR is activated only in the basal part of hypocotyls. Although the pathogen was not detected in cotyledons of type I resistant plants, semiquantitative polymerase chain reaction confirmed the early abundant growth of the pathogen in cotyledons of susceptible plants by 6 days postinfection (dpi). This was in contrast to scarce growth of the pathogen in cotyledons of type II-resistant plants at a later time point (12 dpi). This suggests that pathogen growth differs according to the host–pathogen combination. To get more information about sunflower downy mildew resistance genes, the full-length cDNAs of RGC151 and RGC203, which segregated with the Pl_ARG gene (resistance type I) and Pl₁₄ gene (resistance type II), were cloned and sequenced. Sequence analyses revealed that RGC151 belongs to the Toll/interleukin-1 receptor (TIR) nucleotide-binding site leucine-rich repeat (NBS-LRR) class whereas RGC203 belongs to class coiled-coil (CC)-NBS-LRR. This study suggests that type II resistance may be controlled by CC-NBS-LRR gene transcripts which are enhanced upon infection by P. halstedii, rather than by the TIR-NBS-LRR genes that might control type I resistance.

Additional keywords: incompatible plant–pathogen interactions.