Abstract
Plant-virus interactions are greatly influenced by environmental factors such as temperatures. In virus-infected plants, enhanced temperature is frequently associated with more severe symptoms and higher virus content. However, the mechanisms involved in controlling the temperature regulation of plant-virus interactions are poorly characterised. To elucidate these further, we analysed the responses of potato plants cv Chicago to infection by potato virus Y (PVY) at normal (22 °C) and elevated temperature (28 °C), the latter of which is known to significantly increase plant susceptibility to PVY. Using RNAseq analysis, we showed that single and combined PVY and heat-stress treatments caused dramatic changes in gene expression, affecting the transcription of both protein-coding and non-coding RNAs. Among the newly identified genes responsive to PVY infection, we found genes encoding enzymes involved in the catalysis of polyamine formation and poly ADP-ribosylation. We also identified a range of novel non-coding RNAs which were differentially produced in response to single or combined PVY and heat stress, that consisted of antisense RNAs and RNAs with miRNA binding sites. Finally, to gain more insights into the potential role of alternative splicing and epitranscriptomic RNA methylation during combined stress conditions, direct RNA nanopore sequencing was performed. Our findings offer insights for future studies of functional links between virus infections and transcriptome reprogramming, RNA methylation and alternative splicing.
Highlights
Potato (Solanum tuberosum L.), one of the most important non-grain crops in the world, similar to all other crop plants, is constantly exposed to a plethora of pathogens
In previous work we studied the effect of a moderately elevated temperature (28 ◦C) on the dynamics of Potato virus Y (PVY) infection in potato plants [32], a temperature which mimics the mild heat-stress conditions that may arise as a result of global climate change
An increase in virus titer was observed in the systemically infected leaves of plants grown at 22 ◦C; virus levels were found to be significantly higher in corresponding tissues of plants grown at 28 ◦C [32], suggesting that rising temperature greatly enhances the susceptibility of Chicago plants to PVY
Summary
Potato (Solanum tuberosum L.), one of the most important non-grain crops in the world, similar to all other crop plants, is constantly exposed to a plethora of pathogens Among these pathogens, viruses account for up to 50% of all novel and emerging plant diseases [1]. Potato virus Y (PVY) is one of the most important pathogens of potato, which has a significant negative impact on potato-crop yield and quality [2,3] To help prevent such crop losses, it is essential that we improve plant resistance mechanisms against viruses, which constitutes the most efficient and reliable strategy for plant protection. A second layer of immune response occurs in plants carrying resistance (R or N) genes that employ effector-triggered immunity (ETI) This typically involves the interaction between virus-derived effectors and host resistance R or N (mostly NB-LRR) proteins that trigger a number of intracellular signalling events, which leads to disease resistance [9]. When host defences successfully prevent virus invasion, these types of interaction are referred to as incompatible plant-virus interactions
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