Strategies for integrated deployment of host resistance and fungicides to sustain effective crop protection.

可持续作物保护对粮食安全和确保作物有效利用资源（土地、氮和水）至关重要。杀菌剂和抗病品种是防治大多数作物病害的主要措施。然而，控制对病原体种群施加了选择压力，导致病原体菌株的进化，这些菌株对所使用的杀真菌剂不太敏感，或者能够克服宿主抗性（毒性病原体菌株）。例如，由致病疫霉引起的马铃薯晚疫病是通过喷洒杀真菌剂方案加以防治的，同时在一些马铃薯栽培品种中辅以部分宿主抗性。最近病原菌种群发生了变化：氟啶胺（一种广泛使用的杀真菌剂）的田间药效已被报道，新的抗药性已经发展，导致品种抗性等级下降。综合防治，即采用两种或两种以上的控制措施，被广泛认为是更可持续的，而不是过度依赖于一个控制选项。然而，令人惊讶的是，很少有机制的理解，对病原体进化的影响，组合部署的杀真菌剂和作物抗性基因。杀菌剂不敏感性的演变和毒力的演变是孤立的研究，尽管有很强的理由，他们之间的相互作用的两个过程。新的有毒或耐药菌株比现有的“野生型”菌株具有竞争优势，因为在它们能够克服的控制措施存在的情况下，它们能够比野生型菌株生长得更快。然而，杀真菌剂仍然会减缓新毒株的流行，从而降低其竞争优势。因此，杀真菌剂可能会减缓毒性的选择，并且通过类似的过程，栽培品种抗性可能会减缓杀真菌剂不敏感性的选择。将测试以下假设：H1：作物抗性的部署减少了对杀真菌剂不敏感的选择H2：杀真菌剂的部署减少了对杀真菌剂的选择H3：作物抗性基因和杀真菌剂如何整合是控制持久性的关键决定因素。结果：该项目将使用实验和建模方法来量化将杀真菌剂治疗和品种抗性整合在一起的疾病控制策略的持久性。该项目的直接应用成果是通过马铃薯理事会和行业合作伙伴实施的基于杀菌剂和品种抗性的马铃薯枯萎病战略。进一步的成果是通用的方法来开发，参数化和验证模型，可用于量化综合可持续疾病控制战略的病原体作物systems.This工作是可能的最近在两个领域的进展。首先，在一系列的病原体物种的毒力的变化已被证明是相关的“效应基因”的特征突变。对这些突变的测试允许在田间实验中量化强毒株的比例。然后可以比较处理以测量它们对新菌株选择的影响程度。杀真菌剂不敏感的菌株可以通过类似的方法追踪。其次，流行病学模型已被测试对实验数据，发现给杀菌剂处理的效果，选择不敏感菌株的预测。类似的模型已经被开发出来，代表毒力的演变，它现在是可行的耦合这两种类型的模型来研究综合控制的效果。实地实验将产生流行病学数据和病原体样本。将对样本进行检测，以量化不同处理下强毒株和不敏感毒株频率的变化，从而检验假设1和假设2。由此产生的数据将被用来测试一个耦合的数学模型，然后将被用来探索综合疾病管理战略的假设3。

Sustainable crop protection is of key importance to food security and to ensure that crops make efficient use of resources (land, nitrogen and water). Fungicides and resistant cultivars are the predominant control measures against most crop diseases. However, control imposes a selection pressure on pathogen populations, leading to the evolution of pathogen strains which are less sensitive to the fungicides used or which are able to overcome host resistance (virulent pathogen strains). For example, potato late blight, caused by Phytophthora infestans, is managed by fungicide spray programmes, complemented by partial host resistance in some potato cultivars. Recently the pathogen population has changed: a loss of field efficacy of fluazinam (a widely used fungicide) has been reported, and new virulences have evolved, resulting in downgrading of cultivar resistance ratings.Integrated control, where two or more control measures are applied, is widely believed to be more sustainable than over-reliance on one control option. There is however surprisingly little mechanistic understanding of the effects on pathogen evolution of combining deployment of fungicides and crop resistance genes. The evolution of fungicide insensitivity and the evolution of virulence are studied in isolation, despite a strong rationale for their being interactions between the two processes. New virulent or resistant strains gain a competitive advantage over existing 'wild-type' strains because they are able to grow more rapidly than wild-type strains in the presence of the control measure that they are able to overcome. However, epidemics of a new virulent strain will still be slowed by fungicides, thus reducing its competitive advantage. Hence, fungicides may slow selection for virulence and, by a similar process, cultivar resistance may slow selection for fungicide insensitivity. The following hypotheses will be tested:H1: Deployment of crop resistance reduces selection for fungicide insensitivity.H2: Deployment of fungicides reduces selection for virulence.H3: How crop resistance genes and fungicides are integrated is a key determinant of the durability of control.Outcomes: The project will use experimental and modelling approaches to quantify the durability of disease control strategies integrating fungicide treatments and cultivar resistance. The directly applied outcome of the project is a fungicide and cultivar resistance based strategy for potato blight to be implemented through the Potato Council and industry partners. The further outcomes are generic methods to develop, parameterise and validate models that can be used to quantify integrated sustainable disease control strategies for pathogen-crop systems.This work is made possible by recent progress in two areas. Firstly, changes in virulence in a range of pathogen species have been shown to be related to well characterised mutations in 'effector genes'. Testing for these mutations allows the proportion of virulent strains to be quantified in field experiments. Treatments can then be compared to measure the extent to which they affect selection for new strains. Fungicide insensitive strains can be tracked by similar methods. Secondly, epidemiological models have been tested against experimental data and found to give good predictions of the effect of fungicide treatments on selection for insensitive strains. Similar models have been developed to represent virulence evolution and it is now feasible to couple these two types of model to study the effects of integrated control. Field experiments will generate epidemiological data and pathogen samples. The samples will be tested to quantify changes in the frequency of virulent and insensitive strains, under different treatments, to test hypotheses 1 and 2. The resulting data will be used to test a coupled mathematical model, which will then be used to explore integrated disease management strategies under hypothesis 3.