Cauliflower mosaic virus disease spectrum uncovers novel susceptibility factor NCED9 in Arabidopsis thaliana.

Viruses are intimately linked with their hosts and especially dependent on gene-for-gene interactions to establish successful infections. On the host side, defence mechanisms such as tolerance and resistance can occur within the same species, leading to differing virus accumulation in relation to symptomology and plant fitness. The identification of novel resistance genes against viruses and susceptibility factors is an important part of understanding viral patho-genesis and securing food production. The model plant Arabidopsis thaliana displays a wide symptom spectrum in response to RNA virus infections, and unbiased genome-wide association studies have proven a powerful tool to identify novel disease-genes. In this study we infected natural accessions of A. thaliana with the pararetrovirus cauliflower mosaic virus (CaMV) to study the phenotypic variations between accessions and their correlation with virus accumulation. Through genome-wide association mapping of viral accumulation differences, we identified several susceptibility factors for CaMV, the strongest of which was the abscisic acid synthesis gene NCED9. Further experiments confirmed the importance of abscisic acid homeostasis and its disruption for CaMV disease.

Diverse plant viruses: a toolbox for dissection of cellular pathways.

Research in virology has usually focused on one selected host-virus pathosystem to examine the mechanisms underlying a particular disease. However, as exemplified by the mechanistically versatile suppression of antiviral RNA silencing by plant viruses, there may be functionally convergent evolution. Assuming this is a widespread feature, we propose that effector proteins from diverse plant viruses can be a powerful resource for discovering new regulatory mechanisms of distinct cellular pathways. The efficiency of this approach will depend on how deeply and widely the studied pathway is integrated into viral infections. Beyond this, comparative studies using broad virus diversity should increase our global understanding of plant-virus interactions.

A role of flowering genes in the tolerance of Arabidopsis thaliana to cucumber mosaic virus.

The genetic basis of plant tolerance to parasites is poorly understood. We have previously shown that tolerance of Arabidopsis thaliana to its pathogen cucumber mosaic virus is achieved through changes in host life-history traits on infection that result in delaying flowering and reallocating resources from vegetative growth to reproduction. In this system we analyse here genetic determinants of tolerance using a recombinant inbred line family derived from a cross of two accessions with extreme phenotypes. Three major quantitative trait loci for tolerance were identified, which co-located with three flowering repressor genes, FLC, FRI, and HUA2. The role of these genes in tolerance was further examined in genotypes carrying functional or nonfunctional alleles. Functional alleles of FLC together with FRI and/or HUA2 were required for both tolerance and resource reallocation from growth to reproduction. Analyses of FLC alleles from wild accessions that differentially modulate flowering time showed that they ranked differently for their effects on tolerance and flowering. These results pinpoint a role of FLC in A. thaliana tolerance to cucmber mosaic virus, which is a novel major finding, as FLC has not been recognized previously to be involved in plant defence. Although tolerance is associated with a delay in flowering that allows resource reallocation, our results indicate that FLC regulates tolerance and flowering initiation by different mechanisms. Thus, we open a new avenue of research on the interplay between defence and development in plants.

Salicylic acid and the viral virulence factor 2b regulate the divergent roles of autophagy during cucumber mosaic virus infection.

Macroautophagy/autophagy is a conserved intracellular degradation pathway that has recently emerged as an integral part of plant responses to virus infection. The known mechanisms of autophagy range from the selective degradation of viral components to a more general attenuation of disease symptoms. In addition, several viruses are able to manipulate the autophagy machinery and counteract autophagy-dependent resistance. Despite these findings, the complex interplay of autophagy activities, viral pathogenicity factors, and host defense pathways in disease development remains poorly understood. In the current study, we analyzed the interaction between autophagy and cucumber mosaic virus (CMV) in Arabidopsis thaliana. We show that autophagy is induced during CMV infection and promotes the turnover of the major virulence protein and RNA silencing suppressor 2b. Intriguingly, autophagy induction is mediated by salicylic acid (SA) and dampened by the CMV virulence factor 2b. In accordance with 2b degradation, we found that autophagy provides resistance against CMV by reducing viral RNA accumulation in an RNA silencing-dependent manner. Moreover, autophagy and RNA silencing attenuate while SA promotes CMV disease symptoms, and epistasis analysis suggests that autophagy-dependent disease and resistance are uncoupled. We propose that autophagy counteracts CMV virulence via both 2b degradation and reduced SA-responses, thereby increasing plant fitness with the viral trade-off arising from increased RNA silencing-mediated resistance.

Effective tolerance based on resource reallocation is a virus-specific defence in Arabidopsis thaliana.

Plant viruses often harm their hosts, which have developed mechanisms to prevent or minimize the effects of virus infection. Resistance and tolerance are the two main plant defences to pathogens. Although resistance to plant viruses has been studied extensively, tolerance has received much less attention. Theory predicts that tolerance to low-virulent parasites would be achieved through resource reallocation from growth to reproduction, whereas tolerance to high-virulent parasites would be attained through shortening of the pre-reproductive period. We have shown previously that the tolerance of Arabidopsis thaliana to Cucumber mosaic virus (CMV), a relatively low-virulent virus in this host, accords to these predictions. However, whether other viruses trigger the same response, and how A. thaliana copes with highly virulent virus infections remains unexplored. To address these questions, we challenged six A. thaliana wild genotypes with five viruses with different genomic structures, life histories and transmission modes. In these plants, we quantified virus multiplication, virulence, and the effects of infection on plant growth and reproduction, and on the developmental schedule. Our results indicate that virus multiplication varies according to the virus × host genotype interaction. Conversely, effective tolerance is observed only on CMV infection, and is associated with resource reallocation from growth to reproduction. Tolerance to the other viruses is observed only in specific host-virus combinations and, at odds with theoretical predictions, is linked to longer pre-reproductive periods. These findings only partially agree with theoretical predictions, and contribute to a better understanding of pathogenic processes in plant-virus interactions.