Molecular basis of virulence in tan spot of wheat

小麦核腔菌（Pyrenophora tritici-repentis，Ptr）是小麦褐斑病的病原菌。Ptr的感染导致易感宿主品种的叶子变黄和/或死亡。这些症状反映了坏死营养效应物（内斯）的活性，也称为宿主选择性毒素，其由真菌的种族差异产生。迄今为止已确定了三种内斯：Ptr ToxA、Ptr ToxB和Ptr ToxC。对这些效应物的敏感性通常与对产生它们的真菌的种族的易感性共分离，并且小麦/Ptr相互作用大致遵循宿主-寄生虫关系的逆基因对基因模型，其中病原体分泌的NE和匹配的宿主敏感性基因之间的相互作用导致易感性。然而，近年来，一些数量性状位点和一个主要的显性基因也被确定，赋予小种非特异性抗褐斑病。虽然内斯和匹配的宿主敏感性基因之间的关系在遗传学方面得到了很好的定义，但从分子角度来看，这种相互作用还没有得到很好的理解。这种知识的差距，结合非特异性抗性的证据，建议需要更好地了解参与小麦/Ptr相互作用的分子反应。此外，虽然八个种族的Ptr已被描述的基础上，他们的能力感染一套小麦品种被称为主机差分集，我们假设有额外的种族的真菌，产生的尚未表征的效应控制其毒力概况。我们最近已经确定了许多菌株的Ptr，而类似于现有的种族的基础上，他们引起的症状的差异主机，不编码预期的内斯。伴随着新的种族的Ptr的鉴定，我们还假设，有新的效应介导的相互作用与特定的主机品种。拟议的研究旨在：（1）通过双重RNA-seq方法对小麦/Ptr相互作用进行更广泛的机制理解，同时检测宿主和寄生虫中的转录本，不仅能够评估小麦的分子反应，还能够评估真菌的分子反应转录组;（2）鉴定来自病原体多样性中心北非、新月沃土和中亚的Ptr新小种，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;和（3）在真菌转录组和显示新毒力模式的Ptr分离株的培养物中鉴定候选效应子。本研究将为小麦褐斑病及其相关病害的防治提供重要信息。

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.