Molecular basis of virulence in tan spot of wheat

小麦褐斑病是一种重要的小麦叶斑病。PTR侵染导致感病寄主品种的叶片变黄和/或死亡。这些症状反映了坏死营养效应器(NE)的活性，也被称为宿主选择毒素，这些毒素由真菌的小种不同地产生。到目前为止，已鉴定出三种NE：PTR ToxA、PTR ToxB和PTR ToxC。对这些效应物的敏感性通常与对产生这些效应物的真菌小种的敏感性共分离，小麦/PTR相互作用大致遵循寄主-寄生关系的反向基因对基因模型，其中病原体分泌的NE和匹配的寄主敏感性基因之间的相互作用导致敏感性。然而，近年来也发现了一些数量性状座位和一个主要的显性基因，它们赋予了对褐斑病的小种非特异性抗性。虽然NE和匹配的寄主敏感基因之间的关系在遗传学上得到了很好的定义，但从分子角度来看，这种相互作用并没有得到很好的理解。这些知识上的差距，再加上非特异性抗性的证据，表明有必要更好地理解小麦/PTR相互作用中涉及的分子反应。此外，虽然PTR的八个小种是基于它们感染一系列被称为寄主差异集的小麦品种的能力而被描述的，但我们假设这种真菌还有其他小种，它们产生到目前为止控制其毒力特征的未知效应器。我们最近鉴定了许多PTR分离物，虽然根据它们在不同宿主上引起的症状与现有的小种相似，但不为预期的NE编码。随着PTR新小种的鉴定，我们还假设存在新的效应器来调节与特定寄主品种的相互作用。这项拟议的研究旨在：(1)通过双重RNA-SEQ方法对小麦/PTR相互作用的机制有更广泛的了解，同时检测寄主和寄生虫中的转录本，不仅能够评估小麦的分子反应，还能够评估真菌转录本；(2)通过评估295个硬粒小麦和面包小麦基因型的真菌毒力表型，鉴定来自北非、肥沃的新月会和中亚的PTR新小种，这些小种显示出新的毒力模式；以及(3)在真菌转录本和PTR分离物的培养滤液中确定候选效应因子。这项工作将增加对小麦赤霉病致病因子和致病力、寄主抗性机制和PTR小种结构的认识，为小麦褐斑病及相关病害的防治和了解提供重要信息。

The fungus Pyrenophora tritici-repentis (Ptr) causes tan spot, an important leaf-spotting disease of wheat. Infection by Ptr results in the yellowing and/or death of the leaves of susceptible host varieties. These symptoms reflect the activity of necrotrophic effectors (NEs), also known as host-selective toxins, which are differentially produced by races of the fungus. Three NEs have been identified to date: Ptr ToxA, Ptr ToxB and Ptr ToxC. Sensitivity to these effectors generally co-segregates with susceptibility to the races of the fungus that produce them, and the wheat/Ptr interaction broadly follows the inverse gene-for-gene model of host-parasite relations, in which the interaction between a pathogen-secreted NE and a matching host sensitivity gene results in susceptibility. In recent years, however, several quantitative trait loci and a major dominant gene have also been identified, which confer race-nonspecific resistance to tan spot. While the relationship between the NEs and matching host sensitivity genes is well defined in genetic terms, the interaction is not as well understood from a molecular perspective. Such gaps in knowledge, combined with the evidence of nonspecific resistance, suggest the need for an improved understanding of the molecular responses involved in the wheat/Ptr interaction. Moreover, while eight races of Ptr have been described based on their ability to infect a suite of wheat varieties known as a host differential set, we hypothesize that there are additional races of the fungus, which produce as of yet uncharacterized effectors controlling their virulence profiles. We have recently identified numerous isolates of Ptr that, while resembling existing races based on the symptoms they cause on the differential hosts, do not encode for the expected NEs. Concomitant with the identification of new races of Ptr, we also hypothesize that there occur novel effectors mediating interactions with specific host varieties. The proposed research aims to: (1) develop a broader mechanistic understanding of the wheat/Ptr interaction via a dual RNA-seq approach, simultaneously detecting transcripts in the host and parasite and enabling an assessment not only of the molecular responses of wheat, but also of the fungal transcriptomes; (2) characterize novel races of Ptr from North Africa, the Fertile Crescent and Central Asia, centers of pathogen diversity, by evaluating fungal virulence phenotypes on a collection of 295 durum and bread wheat genotypes; and (3) identify candidate effectors in the fungal transcriptomes and in culture filtrates of isolates of Ptr showing novel virulence patterns. This work will increase knowledge of pathogen effectors and virulence, host resistance mechanisms, and the race structure of Ptr, providing vital information for the management and understanding of tan spot of wheat and related diseases.