持久的抵抗力还是有效的疾病控制?成虫抗性(APR)是这一困境的核心

Loup Rimbaud, Julien Papaïx, Jean-François Rey, Benoît Moury, Luke G. Barrett, Peter H. Thrall
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摘要

成体植物抗性(APR)是植物对病原菌的不完全和延迟保护。乍一看,这种抗性应该不如经典的主效抗性基因有效,后者从苗期起就赋予完全抗性,以减少流行病。然而,通过允许一些“泄漏”水平的疾病,预计APR基因比主要基因更持久,因为它们对病原体施加的适应抗性的选择压力较弱。然而,APR的部分效率和延迟作用方式对耐药性部署的进化和流行病学结果的影响尚未得到检验。本研究首次采用种群遗传学、空间显性、时间随机模型landsepi,在景观尺度上探讨抗性效率、抗性激活时年龄和目标致病性性状如何共同影响抗性持久性和病害防治。我们的数值实验探讨了APR在模拟农业景观中的部署,单独或与主要抗性基因一起。作为一个案例研究,该数学模型已被参数化为谷类作物的锈菌(锈菌属),其中有大量的数据可用。我们的模拟证实,APR基因的低效率和延迟激活降低了病原体的选择压力及其克服抗性的倾向,但不能提供有效的保护。另一方面,较强的APR基因(增加对病原体的选择压力)可能很快被克服,但有可能在短期内提供一些疾病保护。这是由于不同病原体基因型之间的激烈竞争和适应适应度成本的存在,特别是当APR基因通过作物混合或轮作与主要抗性基因一起部署时。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Durable resistance or efficient disease control? Adult Plant Resistance (APR) at the heart of the dilemma
Adult plant resistance (APR) is an incomplete and delayed protection of plants against pathogens. At first glance, such resistance should be less efficient than classical major-effect resistance genes, which confer complete resistance from seedling stage, to reduce epidemics. However, by allowing some ‘leaky’ levels of disease, APR genes are predicted to be more durable than major genes because they exert a weaker selection pressure on pathogens towards adaptation to resistance. However, the impact of partial efficiency and delayed mode of action of APR on the evolutionary and epidemiological outcomes of resistance deployment has never been tested. Using the demogenetic, spatially explicit, temporal, stochastic model landsepi, this study is a first attempt to investigate how resistance efficiency, age at the time of resistance activation and target pathogenicity trait jointly impact resistance durability and disease control at the landscape scale. Our numerical experiments explore the deployment of APR in a simulated agricultural landscape, alone or together with a major resistance gene. As a case study, the mathematical model has been parameterised for rust fungi (genus Puccinia) of cereal crops, for which extensive data are available. Our simulations confirm that weak efficiency and delayed activation of APR genes reduce the selection pressure applied on pathogens and their propensity to overcome resistance, but do not confer effective protection. On the other hand, stronger APR genes (which increase selection pressure on the pathogen) may be quickly overcome but have the potential to provide some disease protection in the short-term. This is attributed to strong competition between different pathogen genotypes and the presence of fitness costs of adaptation, especially when APR genes are deployed together with a major resistance gene via crop mixtures or rotations.
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