Viral fitness predicts the magnitude and direction of perturbations in the infected host transcriptome

Héctor Cervera; Silvia Ambrós; Guillermo P. Bernet; Guillermo Rodrigo; Santiago F. Elena

Thus, we conclude that, at least for the sample of genes here analyzed, the observed correlations between host's gene expression and viral fitness are consistent for both experimental methods used to evaluate the levels of gene expression. The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/206789 doi: bioRxiv preprint regulatory networks. Plant-virus interactions result from the confrontation of two players with opposed strategies and interests. From the plant perspective, activation of basal defenses, immunity, hormone-regulated pathways, and RNA-silencing (some of which are not virusspecific) will result in an immediate benefit to control virus replication and spread. We found that there are plant's defense responses that are expressed upon infection regardless the fitness of the virus, and defense responses induced progressively as viral fitness increases. Consistent with the first mode, we observed the activation of the genes EDS1 and PAD4, components of R genemediated disease resistance with homology to lipases, in every infection studied in this work (Fig. 8A ). These are master regulators of plant defenses that connect pathogen signals with salicylic acid (SA) signaling 53 . SA is involved in resistance to a broad spectrum of pathogens, and in particular viruses 54, 55 . Consistent with the second mode, we observed the activation of many genes involved in defenses in an extent that is proportional to TEV fitness (Fig. 8A ). For example, the DCL2 and AGO1 genes -key for the RNA silencing response-, genes modulating resistance to pathogens such as the subtilisin-like protease (SBT1.9), or genes expressing proteins involved in hormone-regulated defenses such as GASA1 and VQ29, brassinosteroids (e.g., brassinosteroid However, these activations have a cost, mainly in terms of resources that can be invested into secondary metabolism and development. Consistent with this idea is the fact that many genes participating in metabolic processes (e.g., CYSC1, a cysteine synthase) are highly repressed upon infection (Fig. 8A ). There are also central genes for the plant metabolism whose repression correlates with viral fitness, such as GBSS1, photosystem components or assembly factors (e.g., HCF136) , Rubisco subunits and ATPases, catalases, transketolases, nucleotide and phosphate transporters, synthases involved in flavonoid, isoprenoid, ascorbate, or tryptophan biosynthesis, and GAPDH (Fig. 7) .