Tamisier Lucie, Rousseau Elsa, Barraillé Sebastien, Nemouchi Ghislaine, Szadkowski Marion, Mailleret Ludovic, Grognard Frederic, Fabre Frederic, Moury Benoit, Palloix Alain
INRA, UR1052 GAFL, Unité de Génétique et Amélioration des Fruits et Légumes, Domaine St Maurice - 67 Allée des Chênes, CS 60094, F-84143 Montfavet Cedex, France.
INRA, UR407 PV, Unité de Pathologie Végétale, Domaine St Maurice - 67 Allée des Chênes, CS 60094, F-84143 Montfavet Cedex, France.
J Gen Virol. 2017 Jul;98(7):1923-1931. doi: 10.1099/jgv.0.000835. Epub 2017 Jul 8.
Infection of plants by viruses is a complex process involving several steps: inoculation into plant cells, replication in inoculated cells and plant colonization. The success of the different steps depends, in part, on the viral effective population size (Ne), defined as the number of individuals passing their genes to the next generation. During infection, the virus population will undergo bottlenecks, leading to drastic reductions in Ne and, potentially, to the loss of the fittest variants. Therefore, it is crucial to better understand how plants affect Ne. We aimed to (i) identify the plant genetic factors controlling Ne during inoculation, (ii) understand the mechanisms used by the plant to control Ne and (iii) compare these genetic factors with the genes controlling plant resistance to viruses. Ne was measured in a doubled-haploid population of Capsicum annuum. Plants were inoculated with either a Potato virus Y (PVY) construct expressing the green fluorescent protein or a necrotic variant of Cucumber mosaic virus (CMV). Newas assessed by counting the number of primary infection foci on cotyledons for PVY or the number of necrotic local lesions on leaves for CMV. The number of foci and lesions was correlated (r=0.57) and showed a high heritability (h2=0.93 for PVY and h2=0.98 for CMV). The Ne of the two viruses was controlled by both common quantitative trait loci (QTLs) and virus-specific QTLs, indicating the contribution of general and specific mechanisms. The PVY-specific QTL colocalizes with a QTL that reduces PVY accumulation and the capacity to break down a major-effect resistance gene.
病毒对植物的感染是一个复杂的过程,涉及多个步骤:接种到植物细胞、在接种细胞中复制以及在植物中定殖。不同步骤的成功与否部分取决于病毒有效种群大小(Ne),其定义为将基因传递给下一代的个体数量。在感染过程中,病毒种群会经历瓶颈效应,导致Ne急剧减少,并可能导致最适应的变异体丢失。因此,更好地了解植物如何影响Ne至关重要。我们旨在:(i)确定接种过程中控制Ne的植物遗传因素;(ii)了解植物控制Ne所使用的机制;(iii)将这些遗传因素与控制植物对病毒抗性的基因进行比较。在辣椒的双单倍体群体中测量了Ne。用表达绿色荧光蛋白的马铃薯Y病毒(PVY)构建体或黄瓜花叶病毒(CMV)的坏死变体接种植物。对于PVY,通过计算子叶上的初次感染病灶数量来评估Ne;对于CMV,则通过计算叶片上坏死局部病斑的数量来评估Ne。病灶和病斑的数量具有相关性(r = 0.57),并且显示出高遗传力(PVY的h2 = 0.93,CMV的h2 = 0.98)。两种病毒的Ne均由常见的数量性状位点(QTL)和病毒特异性QTL控制,这表明了一般机制和特定机制的作用。PVY特异性QTL与一个QTL共定位,该QTL可减少PVY积累以及分解一个主效抗性基因的能力。