Molecular basis of virulence in Pyrenophora tritici-repentis

小麦核腔菌（Pyrenophora tritici-repentis）会引起褐斑病，这是一种叶斑病，在小麦生长过程中的任何时候都会对小麦造成损害。 据估计，棕褐色斑点会使产量减少2- 15%，尽管据报道损失高达50%。 被小麦疫霉感染导致在易感植物的叶子上形成损伤或斑点，其由死亡（坏死）和/或黄色（褪绿）组织组成。 这些症状是由真菌产生的寄主选择性毒素引起的，这些毒素可以影响一些小麦品种，但对其他品种没有影响。 三种寄主选择性毒素，称为Ptr ToxA、Ptr ToxB和Ptr ToxC，由小麦疫霉菌株单独或组合产生。这三种毒素对褐斑病的发展都很重要，真菌需要产生至少一种毒素才能在特定的小麦品种上引起疾病。然而，除了需要引起疾病之外，Ptr ToxB还存在剂量效应，这意味着较高水平的Ptr ToxB导致易感小麦上更严重的疾病症状。由真菌菌株产生的Ptr ToxB的量反映了该菌株中ToxB基因（编码毒素）的拷贝数，以及这些拷贝的表达活性。 尽管它在褐斑发展中的重要性，但目前尚不清楚为什么产生Ptr ToxB的真菌菌株在加拿大极其罕见，而产生Ptr ToxA的真菌菌株却非常常见。 类似地，目前还不知道ToxB基因的多个拷贝是否发生在携带其他重要基因的染色体上，因此对真菌是必需的，或者它是否发生在对真菌的生存不是必需的但对致病性或其他专门功能是必需的条件性染色体上。 拟议的研究将：1）通过比较产生Ptr ToxB和Ptr ToxA的真菌菌株的竞争能力，帮助确定ToxB的流行病学意义，2）评估ToxB的拷贝如何排列以及它们是否出现在必需或非必需染色体上，以及3）确定小麦假单胞菌菌株之间以及与密切相关物种之间融合的性质，这可以解释某些菌株是如何获得宿主选择性毒素的。 这项工作的目的是增加知识的基础和演变的P. tritici-repentis的毒力，并提供重要的信息，以评估和减轻未来的棕斑病流行的风险。 通过了解真菌如何引起疾病，以及它如何变得致病，我们可以制定更积极有效的疾病管理策略。 这反过来将减少加拿大农民的产量和经济损失。

The fungus Pyrenophora tritici-repentis causes tan spot, a leaf spotting disease that can damage growing wheat anytime during its development. Tan spot is estimated to reduce yield by between 2-15%, although losses as high as 50% have been reported. Infection by P. tritici-repentis causes the formation of lesions or spots on the leaves of susceptible plants, which consist of dead (necrotic) and/or yellow (chlorotic) tissue. These symptoms result from the production, by the fungus, of host-selective toxins that can affect some wheat varieties but not others. Three host-selective toxins, termed Ptr ToxA, Ptr ToxB and Ptr ToxC, are produced alone or in combination by strains of P. tritici-repentis. All three toxins are important for tan spot development, and the fungus needs to produce at least one of them to be able to cause disease on specific wheat varieties. In addition to being required to cause disease, however, there is also a dosage effect of Ptr ToxB, meaning that higher levels of Ptr ToxB result in more severe disease symptoms on susceptible wheat. The amount of Ptr ToxB that is produced by a fungal strain reflects the number of copies of the ToxB gene (which codes for the toxin) in that strain, as well as how actively those copies are expressed.   Despite its importance in tan spot development, it is not clear why fungal strains that produce Ptr ToxB are extremely rare in Canada, while those that produce Ptr ToxA are very common. Similarly, it is not known whether the multiple copies of the ToxB gene occur on a chromosome that carries other important genes, and is therefore essential to the fungus, or whether it occurs on a conditionally dispensable chromosome that is not essential for survival of the fungus, but is necessary for pathogenicity or other specialized functions. The proposed research will: 1) help to determine the epidemiological significance of ToxB by comparing the competitive ability of fungal strains that produce Ptr ToxB and Ptr ToxA, 2) evaluate how copies of ToxB are arranged and if they occur on an essential or dispensable chromosome, and 3) determine the nature of fusion between strains of P. tritici-repentis with each other and with closely related species, which could explain how certain strains obtained the host-selective toxins in the first place. The aim of this work is to increase knowledge of the basis for and evolution of virulence in P. tritici-repentis, and to provide information vital to assessing and mitigating the risk of future tan spot epidemics. By understanding how a fungus causes disease, and how it can become pathogenic, we can develop more proactive and effective disease management strategies. This in turn will reduce the yield and economic losses incurred by Canadian farmers.