Tobacco necrosis virus A overcomes local cell death response in Nicotiana tabacum

被引:2
|
作者
Garcia, Lucila [1 ,2 ]
Gerhardt, Nadia [1 ,2 ]
Martin, Ana P. [1 ]
Martinez, Maria F. [1 ]
Alemano, Sergio [3 ]
Marano, Maria R. [1 ,2 ]
机构
[1] Consejo Nacl Invest Cient & Tecnol CONICET, Inst Biol Mol & Celular Rosario IBR, Ocampo & Esmeralda S-N, Rosario, Argentina
[2] Univ Nacl Rosario UNR, Fac Ciencias Bioquim & Farmaceut, Area Virol, Rosario, Argentina
[3] Univ Nacl Rio Cuarto, Fac Ciencias Exactas Fis Quim & Nat, Lab Fisiol Vegetal, Cordoba, Argentina
关键词
alphanecrovirus; local necrotic lesion; pathogen-associated molecular patterns (PAMPs); salicylic acid; SGT1; unfolded protein response (UPR); SALICYLIC-ACID; HYPERSENSITIVE RESPONSE; DISEASE RESISTANCE; SYSTEMIC NECROSIS; UNFOLDED PROTEIN; COAT PROTEIN; MOSAIC-VIRUS; GENE; SGT1; HOST;
D O I
10.1111/ppa.13629
中图分类号
S3 [农学(农艺学)];
学科分类号
0901 ;
摘要
Tobacco necrosis virus A (TNVA) belongs to the genus Alphanecrovirus in the Tombusviridae family. Symptoms induced by TNVA include necrotic lesions on inoculated leaves in a wide host range. The necrotic cell death response to certain viruses is poorly understood. This study characterizes the mechanisms underlying the local cell death triggered by TNVA in Nicotiana tabacum, showing that it shares several components with the hypersensitive response (HR) mediated by resistance proteins. TNVA perception triggers the accumulation of local viral-derived small interference RNA and the regulation of biological processes related to pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), including hydrogen peroxide accumulation, cell wall reinforcement, the activation of unfolded protein response and the induction of salicylic acid (SA) and SA-dependent pathways. However, these antiviral defences do not prevent either local virus multiplication or systemic movement, leading to disease development. Nevertheless, SA-deficient NahG tobacco plants challenged with TNVA showed an increase in virus accumulation on noninoculated leaves, which was correlated with the development of systemic necrosis, highlighting the role of SA signalling in TNVA-induced defence. In addition, SA treatment enhanced the local defence response to TNVA infection and suppressed systemic necrosis in N. benthamiana. Taken together, our data suggest that TNVA induces an impaired plant defence response by modulating host factors to persist at low levels in distal tissues.
引用
收藏
页码:154 / 169
页数:16
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