5 research outputs found

    Impact de la dérive génétique sur l'adaptation d'un virus de plante à des mécanismes quantitatifs de résistance chez son hÎte

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    MasterGenetic resistances in crops allow an efficient control of viruses but may be compromised by virus resistance breakdown ability. Patata virus Y (PVY) can break the major resistance gene pvr23 in pepper (Capsicum annuum L.) but the plant genetic background can improve the major resistance gene durability. I have shawn that three QTL (quantitative trait loci) in pepper, located on chromosomes 6, 7 and 12, tend to lower the number ofPVY primary infection foci on the inoculated cotyledons. These QTL could lower the effective population size (Ne) of the virus during the inoculation step and improve the effect of genetic drift during this step. This mechanism could, in the same way, contribute to improve the durability of pvr23 by lowering the probability of transmission of a virulent variant already present in the inoculum and/or by delaying the appearance of the viral virulent variants in the resistant plant.Les rĂ©sistances gĂ©nĂ©tiques dans les plantes cultivĂ©es permettent de lutter efficacement contre les virus mais peuvent ĂȘtre compromises par les capacitĂ©s de contournement de ces virus. Le virus Y de la pomme de terre (PVY) peut contourner le gĂšne majeur de rĂ©sistance pvr23 chez le piment (Capsicum annuum L.) mais le fond gĂ©nĂ©tique chez la plante peut amĂ©liorer la durabilitĂ© de ce gĂšne majeur de rĂ©sistance. J'ai montrĂ© que trois QTL (quantitative trait loci) prĂ©sents sur les chromosomes 6, 7 et 12 du piment permettent de diminuer le nombre de foyers primaires d'infection du PVY au niveau des organes inoculĂ©s. L'effet de ces QTL pourrait permettre de diminuer la taille efficace de la population (Ne) virale lors de l'inoculation et augmenter l'effet de la dĂ©rive gĂ©nĂ©tique Ă  cette Ă©tape. Ce mĂ©canisme pourrait, partiellement, contribuer Ă  amĂ©liorer la durabilitĂ© du gĂšne pvr23 en diminuant la probabilitĂ© qu'un variant virulent prĂ©sent dans la population virale inoculĂ©e soit transmis et/ou en retardant l'apparition de variants viraux virulents chez la plante rĂ©sistante

    Impact of quantitative plant resistance on within-host viral demo-genetic dynamics

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    International audienceThe deployment of virus-resistant plant crops often leads to the emergence of resistance-breaking pathogens that suppress the yield benefit provided by the resistance. Although breakdowns are well understood for qualitative resistance to crop pests, especially for viruses, they remain to be studied in the case of quantitative resistance. Furthermore, the advantage of quantitative resistance in terms of sustainable management has been proved. The purpose of the ongoing work presented here is to analyze the effect of quantitative resistance on the within-host demo-genetic dynamics of plant viruses by combining experimentation and modelling. The infection of a plant by a virus is a multi-step process starting from inoculation, followed by leaf colonization, and then by systemic infection. At each of these steps, bottlenecks can occur. In turn, genetic drift and selection impact the demo-genetic dynamics of viral populations with varying intensities. Moreover, the size of the bottlenecks is likely to depend on host genetic factors, such as quantitative plant resistance. Here, we aim to quantify the size of these bottlenecks and then to infer the strength of genetic drift and selection operating at each step, for several systems of quantitative resistance in pepper progenies infected with Potato virus Y (PVY)

    Quantitative trait loci in pepper genome control the effective population size of two RNA viruses at inoculation

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    International audienceInfection of plants by viruses is a complex process that involves several steps: inoculation into plant cells, replication in inoculated cells, cell-to-cell movement during leaf colonization and long-distance movement during systemic infection. The success of the different steps is conditioned by the effective viral population size (Ne) defined as the number of individuals that pass their genes to the next generation. During the infection cycle, the virus population will endure several bottlenecks leading to drastic reductions in Ne and to the random loss of sorne virus variants. If strong enough, these bottlenecks could act against selection by eliminating the fittest variants. Therefore, a better understanding of how plant affects Ne rnay contribute to the developrnent of durable virus-resistant cultivars. We aimed to (i) identify plant genetic factors that control Ne at the inoculation step, (ii) understand the mechanisms used by the plant to control Ne and (iii) compare these genetic factors with other genes controlling virus life cycle and plant resistance durability. The virus effective population size was measured in a segregating population of 152 doubled-haploid lines of Capsicum annuum. Plants were inoculated mechanically either with a Patata virus Y (PVY) construct expressing the green fluorescent protein (OFP), or a necrotic variant of Cucumber mosaic virus (CMV), the CMV-N strain of Fulton. Ne was assessed by counting the number ofprimary infection foci observed on inoculated cotyledons under UV light for PVY -OFP or the number of necrotic local lesionsobserved on inoculated leaves for CMY-N. The numbers of primary infection foci and locallesions were correlated arnong the doubled-haploid lines (r=0.57) and showed a high heritability (h2=0.93 and 0.98 for PVY and CMV, respectively). The effective population size of the two viruses was shown to be controlled by botb common quantitative trait loci (QTLs) and virus-specifie QTLs, indicating the contribution ofboth general and specifie mechanisms. The PVY-specific QTL colocalizes with a QTL that had previously been shown to be involved in PVY accumulation and capacity to break amajor-effect resistance gene down

    Quantitative trait loci in pepper control the effective population size of two RNA viruses at inoculation

    No full text
    International audienceInfection 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
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