National Soybean Research Center, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
Phytopathology. 2011 Aug;101(8):970-9. doi: 10.1094/PHYTO-06-10-0163.
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 PlARG 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.
根据宿主-病原菌组合的不同，先前已经确定了向日葵-菌核盘菌两种不亲和反应类型。I 型抗性可以限制病原菌在下胚轴基部的生长，而 II 型则不能，从而允许病原菌到达子叶。在 II 型抗性中，病原菌侵入大部分下胚轴，随后在较长的下胚轴部分激活过敏反应（HR）。因此，与 I 型抗性相比，II 型抗性中的 HR 伴随着 hsr203j 向日葵同源物的更高诱导，其中 HR 仅在下胚轴基部被激活。尽管在 I 型抗性植物的子叶中未检测到病原菌，但半定量聚合酶链反应证实，在感染后 6 天（dpi），易感植物子叶中的病原菌早期大量生长。这与 II 型抗性植物子叶中病原菌后期生长稀少形成对比（12 dpi）。这表明病原菌的生长方式因宿主-病原菌组合而异。为了获得更多关于向日葵霜霉病抗性基因的信息，与 PlARG 基因（I 型抗性）和 Pl14 基因（II 型抗性）分离的 RGC151 和 RGC203 的全长 cDNA 被克隆并测序。序列分析表明，RGC151 属于 Toll/白细胞介素-1 受体（TIR）核苷酸结合位点富含亮氨酸重复（NBS-LRR）类，而 RGC203 属于卷曲螺旋（CC）-NBS-LRR 类。这项研究表明，II 型抗性可能由 CC-NBS-LRR 基因转录本控制，这些转录本在被 P. halstedii 感染后增强，而不是由可能控制 I 型抗性的 TIR-NBS-LRR 基因控制。
