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定量抗性可能导致抗性 QTL 未靶向的性状发生进化变化。

Quantitative resistance can lead to evolutionary changes in traits not targeted by the resistance QTLs.

机构信息

Department of Computational and Systems Biology, Rothamsted Research Harpenden, Hertfordshire, UK.

INRA, UMR 1290 Bioger Thiverval Grignon, France.

出版信息

Evol Appl. 2014 Mar;7(3):370-80. doi: 10.1111/eva.12130. Epub 2014 Jan 2.

DOI:10.1111/eva.12130
PMID:24665339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3962297/
Abstract

This paper addresses the general concern in plant pathology that the introduction of quantitative resistance in the landscape can lead to increased pathogenicity. Hereto, we study the hypothetical case of a quantitative trait loci (QTL) acting on pathogen spore production per unit lesion area. To regain its original fitness, the pathogen can break the QTL, restoring its spore production capacity leading to an increased spore production per lesion. Or alternatively, it can increase its lesion size, also leading to an increased spore production per lesion. A data analysis shows that spore production per lesion (affected by the resistance QTL) and lesion size (not targeted by the QTL) are positively correlated traits, suggesting that a change in magnitude of a trait not targeted by the QTL (lesion size) might indirectly affect the targeted trait (spore production per lesion). Secondly, we model the effect of pathogen adaptation towards increased lesion size and analyse its consequences for spore production per lesion. The model calculations show that when the pathogen is unable to overcome the resistance associated QTL, it may compensate for its reduced fitness by indirect selection for increased pathogenicity on both the resistant and susceptible cultivar, but whereby the QTLs remain effective.

摘要

本文探讨了植物病理学中的一个普遍关注问题,即引入景观中的定量抗性可能会导致病原体致病性增加。为此,我们研究了一个假设情况,即一个作用于单位病斑面积上病原体孢子产生数量的数量性状位点(QTL)。为了恢复其原始适应性,病原体可以打破 QTL,从而恢复其孢子产生能力,导致每个病斑的孢子产生量增加。或者,它可以增加其病斑大小,也会导致每个病斑的孢子产生量增加。数据分析表明,每个病斑的孢子产生量(受抗性 QTL 影响)和病斑大小(不受 QTL 靶向)是正相关的性状,这表明未被 QTL 靶向的性状(病斑大小)的幅度变化可能会间接影响靶向性状(每个病斑的孢子产生量)。其次,我们对病原体适应增加病斑大小的影响进行建模,并分析其对每个病斑的孢子产生量的后果。模型计算表明,当病原体无法克服与抗性相关的 QTL 时,它可能会通过对抗性和易感品种的间接选择来增加致病性,从而弥补其适应性降低,但 QTL 仍然有效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/70efe8ed9273/eva0007-0370-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/55a445dc2662/eva0007-0370-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/81bc6f91b091/eva0007-0370-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/7a43ab5c060b/eva0007-0370-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/70efe8ed9273/eva0007-0370-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/55a445dc2662/eva0007-0370-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/81bc6f91b091/eva0007-0370-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/7a43ab5c060b/eva0007-0370-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f527/3962297/70efe8ed9273/eva0007-0370-f4.jpg

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