Tobacco mosaic virus infection of Nicotiana benthamiana induces salicylic acid glucosyltransferase gene expression associated with lethal systemic necrosis
TL;DR
It is suggested that strong induction of SAGT expression may interfere with SA-mediated defensive responses necessary for suppression of lethal symptoms in WtNb infected with TMV.
Abstract
In wild-type Nicotiana benthamiana (WtNb), tobacco mosaic virus (TMV) causes systemic leaf curling, chlorosis/wilting, and eventually necrosis/plant death. Here, we discovered a possible role of the salicylic acid glucosyltransferase gene (SAGT) in lethal TMV–WtNb interactions. SAGT-suppressed Nb (IR) lines had a lower disease index than WtNb and SAGT-overexpressing Nb (OE) lines did. Treatment with benzothiadiazole, which has a suppressive effect on SAGT transcription in WtNb, substantially delayed or abolished systemic necrosis/plant death, but treatment with SA or water did not. Before onset of systemic chlorosis, WtNb and OE lines inoculated with TMV had much higher levels of SAGT transcripts than in IR lines. Among WtNb and all the transgenic lines, IR lines had the highest levels of transcripts for the pathogenesis-related protein 1a gene and the lowest level of TMV. These results suggest that strong induction of SAGT expression may interfere with SA-mediated defensive responses necessary for suppression of lethal symptoms in WtNb infected with TMV.