title: Viral-induced systemic necrosis in plants involves both programmed cell death and the inhibition of viral multiplication, which are regulated by independent pathways.
abstract: Resistant plants respond rapidly to invading avirulent plant viruses by triggering a hypersensitive response (HR). An HR is accompanied by a restraint of virus multiplication and programmed cell death (PCD), both of which have been observed in systemic necrosis triggered by a successful viral infection. Here, we analyzed signaling pathways underlying the HR in resistance genotype plants and those leading to systemic necrosis. We show that systemic necrosis in Nicotiana benthamiana, induced by Plantago asiatica mosaic virus (PlAMV) infection, was associated with PCD, biochemical features, and gene expression patterns that are characteristic of HR. The induction of necrosis caused by PlAMV infection was dependent on SGT1, RAR1, and the downstream mitogen-activated protein kinase (MAPK) cascade involving MAPKKKalpha and MEK2. However, although SGT1 and RAR1 silencing led to an increased accumulation of PlAMV, silencing of the MAPKKKalpha-MEK2 cascade did not. This observation indicates that viral multiplication is partly restrained even in systemic necrosis induced by viral infection, and that this restraint requires SGT1 and RAR1 but not the MAPKKKalpha-MEK2 cascade. Similarly, although both SGT1 and MAPKKKalpha were essential for the Rx-mediated HR to Potato virus X (PVX), SGT1 but not MAPKKKalpha was involved in the restraint of PVX multiplication. These results suggest that systemic necrosis and HR consist of PCD and a restraint of virus multiplication, and that the latter is induced through unknown pathways independent from the former.
authors.affiliation: Laboratory Of Plant Pathology, Department Of Agricultural And Environmental Biology, Graduate School Of Agricultural And Life Sciences, The University Of Tokyo, Tokyo, Japan.
authors.forename: Ken
authors.initials: K
authors.lastname: Komatsu
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Hashimoto
authors.forename: Johji
authors.initials: J
authors.lastname: Ozeki
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Yamaji
authors.forename: Kensaku
authors.initials: K
authors.lastname: Maejima
authors.forename: Hiroko
authors.initials: H
authors.lastname: Senshu
authors.forename: Misako
authors.initials: M
authors.lastname: Himeno
authors.forename: Yukari
authors.initials: Y
authors.lastname: Okano
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kagiwada
authors.forename: Shigetou
authors.initials: S
authors.lastname: Namba
mesh_terms: D017209:Apoptosis; D015152:Blotting, Northern; D018506:Gene Expression Regulation, Plant; D015967:Gene Expression Regulation, Viral; D054884:Host-Pathogen Interactions; D007113:Immunity, Innate / Q000235:genetics; D015151:Immunoblotting; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D009336:Necrosis; D010935:Plant Diseases / Q000235:genetics / Q000821:virology; D018515:Plant Leaves / Q000235:genetics / Q000502:physiology / Q000821:virology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D010943:Plantago / Q000821:virology; D017863:Potexvirus / Q000235:genetics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*; D014026:Nicotiana / Q000235:genetics / Q000502:physiology / Q000821:virology; D014779:Virus Replication / Q000235:genetics / Q000502:physiology*
chemical_list: D010940:Plant Proteins; D020928:Mitogen-Activated Protein Kinases