Identification of MAPKs as signal transduction components required for the cell death response during compatible infection by the synergistic pair Potato virus X-Potato virus Y

Systemic necrosis is one of the most severe symptoms caused in compatible plant-virus interactions and shares common features with the hypersensitive response (HR). Mitogen-activated protein kinase (MAPK) cascades are associated with responses to compatible and incompatible host-virus interactions. Here, we show that virus-induced gene silencing of the Nicotiana benthamiana MAPK genes salicylic acid-induced protein kinase (SIPK) and wound-induced protein kinase (WIPK), and the MAPK kinase (MAPKK) genes MEK1 and MKK1, partially compromised the HR-like response induced by the synergistic interaction of Potato virus X with Potato virus Y (PVX-PVY). Nevertheless, ameliorated cell death induced by PVX-PVY in the MAPK(K)-silenced plants did not facilitate virus accumulation in systemically infected leaves. Dual silencing of SIPK and of the oxylipin biosynthetic gene 9-Lipoxygenase showed that the latter was epistatic to SIPK in response to PVX-PVY infection. These findings demonstrate that SIPK, WIPK, MEK1 and MKK1 function as positive regulators of PVX-PVY-induced cell death.