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

可持续的作物保护对于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，控制对病原菌种群施加了选择压力，导致对所用杀菌剂不太敏感或能够克服寄主抗性的病原菌菌株(毒力病原菌菌株)的进化。例如，由马铃薯晚疫病菌引起的马铃薯晚疫病是通过杀菌剂喷洒计划进行管理的，并在一些马铃薯品种中辅以部分寄主抗性。最近，病原菌种群发生了变化：据报道，广泛使用的杀菌剂氟嗪南失去了田间药效，新的毒力已经进化，导致品种抗药性等级下降。人们普遍认为，采用两种或两种以上防治措施的综合防治比过度依赖一种防治方法更可持续。然而，令人惊讶的是，关于联合使用杀菌剂和作物抗性基因对病原菌进化的影响，机制上的了解很少。杀菌剂不敏感性的进化和毒力的进化被孤立地研究，尽管它们是这两个过程之间相互作用的强有力的理论基础。新的毒力或抗药性菌株比现有的“野生型”菌株获得了竞争优势，因为在它们能够克服的控制措施的存在下，它们能够比野生型菌株生长得更快。然而，一种新的毒力菌株的流行仍将因杀菌剂而减缓，从而降低其竞争优势。因此，杀菌剂可能会减缓对毒性的选择，通过类似的过程，品种抗性可能会减缓对杀菌剂不敏感的选择。将检验以下假设：H1：部署作物抗性减少对杀菌剂不敏感的选择。H2：部署杀菌剂减少对毒力的选择。H3：作物抗性基因和杀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模拟方法来量化结合杀菌剂处理和品种抗性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疫病战略。进一步的成果是开发、参数化和验证模型的通用方法，这些模型可以用于量化病原-作物系统的综合可持续疾病控制策略。这项工作因两个领域的最新进展而成为可能。首先，一系列病原体物种的毒力变化已被证明与“效应器基因”的特征突变有关。对这些突变的检测可以在现场实验中量化毒力菌株的比例。然后可以对处理进行比较，以衡量它们对新菌株选择的影响程度。对杀菌剂不敏感的菌株可以用类似的方法进行追踪。其次，流行病学模型已经根据实验数据进行了测试，发现可以很好地预测杀菌剂治疗对选择不敏感菌株的影响。已经开发了类似的模型来表示毒力进化，现在可以将这两种类型的模型结合起来研究综合防治的效果。现场实验将产生流行病学数据和病原体样本。这些样本将被测试，以量化在不同处理下毒力和不敏感菌株的频率变化，以检验假设1和假设2。结果数据将用于测试一个耦合的数学模型，然后将用于探索假设3下的综合疾病管理策略。

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.