Abstract
BackgroundPotato virus Y (PVY) is a major pathogen that causes substantial economic losses in worldwide potato production. Different potato cultivars differ in resistance to PVY, from severe susceptibility, through tolerance, to complete resistance. The aim of this study was to better define the mechanisms underlying tolerant responses of potato to infection by the particularly aggressive PVYNTN strain. We focused on the dynamics of the primary metabolism-related processes during PVYNTN infection.ResultsA comprehensive analysis of the dynamic changes in primary metabolism was performed, which included whole transcriptome analysis, nontargeted proteomics, and photosynthetic activity measurements in potato cv. Désirée and its transgenic counterpart depleted for accumulation of salicylic acid (NahG-Désirée). Faster multiplication of virus occurred in the NahG-Désirée, with these plants developing strong disease symptoms. We show that while the dynamics of responses at the transcriptional level are extensive and bimodal, this is only partially translated to the protein level, and to the final functional outcome. Photosynthesis-related genes are transiently induced before viral multiplication is detected and it is down-regulated later on. This is reflected as a deficiency of the photosynthetic apparatus at the onset of viral multiplication only. Interestingly, specific and constant up-regulation of some RuBisCO transcripts was detected in Désirée plants, which might be important, as these proteins have been shown to interact with viral proteins.In SA-deficient and more sensitive NahG-Désirée plants, consistent down-regulation of photosynthesis-related genes was detected. A constant reduction in the photochemical efficiency from the onset of viral multiplication was identified; in nontransgenic plants this decrease was only transient. The transient reduction in net photosynthetic rate occurred in both genotypes with the same timing, and coincided with changes in stomatal conductivity.ConclusionsDown-regulation of photosynthesis-related gene expression and decreased photosynthetic activity is in line with other studies that have reported the effects of biotic stress on photosynthesis. Here, we additionally detected induction of light-reaction components in the early stages of PVYNTN infection of tolerant interaction. As some of these components have already been shown to interact with viral proteins, their overproduction might contribute to the absence of symptoms in cv. Désirée.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1925-2) contains supplementary material, which is available to authorized users.
Highlights
Potato virus Y (PVY) is a major pathogen that causes substantial economic losses in worldwide potato production
We show that while the dynamics of responses at the transcriptional level are extensive and bimodal, this is only partially translated to the protein level, and to the final functional outcome
Désirée compared to mock-inoculated plants was slightly more yellowing of the inoculated leaves starting at 7 days post inoculation (Additional file 1A)
Summary
Potato virus Y (PVY) is a major pathogen that causes substantial economic losses in worldwide potato production. Different potato cultivars differ in resistance to PVY, from severe susceptibility, through tolerance, to complete resistance. Potato virus Y (PVY) is a member of the Potyviridae family, and economically, it is one of the most important potato pathogens, with a worldwide spread [1]. PVYNTN is an aggressive isolate that induces severe symptoms in sensitive potato cultivars, with the development of potato tuber necrotic ringspot disease, resulting in major economic losses [2, 3]. Different potato cultivars show different levels of sensitivity to this particular viral strain, from susceptibility, through tolerance, to complete resistance (reviewed in [2]). It has become clear that plant defense responses are complex, and that they arise from crosstalk between different hormonal signaling pathways that enable specificity of responses to different pathogens and fine-tuning of defense responses [5, 9]
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