Ethylene Signaling Pathway Is Required for AAL-Toxin-Induced Programmed Cell Death.

Abstract

AAL-toxin is a pathogenicity factor of Alternaria alternate f. sp. lycopersici. Little is known about the signaling pathway of AAL-toxin leading to programmed cell death. To investigate candidate genes involved in AAL-toxin-induced cell death, we used virus-induced gene silencing (VIGS) and Nicotiana umbratica that is sensitive to the AAL-toxin. VIGS analyses indicated that AAL-toxin-induced cell death requires for a mitogen-activated protein kinase kinase, MEK2 that is involved in the ethylene synthesis, and the ethylene signaling components, EIN2 and EIN3, suggesting that ethylene biosynthesis and the downstream signaling are required for AAL-toxin-induced cell death. However, EIN2 and EIN3 were not required for HR cell death induced by INF1 elicitor or MEK2^DD. We identified an ERF gene involved in AAL-toxin induced cell death. Overexpression of the ERF did not induce the cell death, suggesting that ethylene signaling is necessary, but not sufficient for AAL-toxin-induced cell death.