Abstract
Cauliflower mosaic virus (CaMV) encodes a multifunctional protein P6 that is required for translation of the 35S RNA and also acts as a suppressor of RNA silencing. Here we demonstrate that P6 additionally acts as a pathogenicity effector of an unique and novel type, modifying NPR1 (a key regulator of salicylic acid (SA)- and jasmonic acid (JA)-dependent signaling) and inhibiting SA-dependent defence responses We find that that transgene-mediated expression of P6 in Arabidopsis and transient expression in Nicotiana benthamiana has profound effects on defence signaling, suppressing expression of representative SA-responsive genes and increasing expression of representative JA-responsive genes. Relative to wild-type Arabidopsis P6-expressing transgenics had greatly reduced expression of PR-1 following SA-treatment, infection by CaMV or inoculation with an avirulent bacterial pathogen Pseudomonas syringae pv tomato (Pst). Similarly transient expression in Nicotiana benthamiana of P6 (including a mutant form defective in translational transactivation activity) suppressed PR-1a transcript accumulation in response to Agrobacterium infiltration and following SA-treatment. As well as suppressing the expression of representative SA-regulated genes, P6-transgenic Arabidopsis showed greatly enhanced susceptibility to both virulent and avirulent Pst (titres elevated 10 to 30-fold compared to non-transgenic controls) but reduced susceptibility to the necrotrophic fungus Botrytis cinerea. Necrosis following SA-treatment or inoculation with avirulent Pst was reduced and delayed in P6-transgenics. NPR1 an important regulator of SA/JA crosstalk, was more highly expressed in the presence of P6 and introduction of the P6 transgene into a transgenic line expressing an NPR1:GFP fusion resulted in greatly increased fluorescence in nuclei even in the absence of SA. Thus in the presence of P6 an inactive form of NPR1 is mislocalized in the nucleus even in uninduced plants. These results demonstrate that P6 is a new type of pathogenicity effector protein that enhances susceptibility to biotrophic pathogens by suppressing SA- but enhancing JA-signaling responses.
Highlights
It is a paradigm that any micro-organism that functions as an effective pathogen must possess mechanisms either to suppress or evade the armoury of host defence responses
To test if P6 might be interfering with Salicylic Acid (SA)-signaling during Cauliflower mosaic virus (CaMV) infection we inoculated transgenic Arabidopsis plants which constitutively expresses high levels of P6 [28] with CaMV, and compared the expression of PR-1 [10,31] with CaMV-infected non-transgenic (NT) plants in the same ecotypic (Ler) background
Transcripts were measured by Real Time qPCR in samples harvested at 14 dpi a time at which we have previously showed that SAresponsive markers are strongly up-regulated in CaMV-infected wild-type plants [14]
Summary
It is a paradigm that any micro-organism that functions as an effective pathogen must possess mechanisms either to suppress or evade the armoury of host defence responses. This is true for biotrophic plant pathogens because they can only maintain a successful infection in the presence of living host cells. Plant viruses are amongst the least genetically complex pathogens but must maintain the ability to overcome host-defences. Much recent attention has focused on the role of RNA-silencing in anti-virus defence and the majority of plant viruses encode silencing suppressor proteins (VSSPs) [4]. Exogenous application of SA or analogues can reduce accumulation or long-distance movement of a number of viruses, e.g. Tobacco mosaic virus (TMV)
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