Two ways to die: Species dependent PCD modes in grapevine cells.

Programmed cell death (PCD) is considered as a hallmark of strain-specific immunity. In contrast, generic basal immunity is thought to act without PCD. This classical bifurcation has been questioned during recent years. Likewise, the role of jasmonate signalling for these two modes of innate immunity has remained ambiguous. We have addressed both questions using two closely related grapevine cell lines (V. rupestris, V. vinifera cv. 'Pinot Noir') that contrast in their cell-death response to the bacterial elicitor harpin and the hormonal trigger methyl jasmonate (MeJA). We follow different cellular (loss of membrane integrity, mortality), molecular (induction of transcripts for phytoalexin synthesis and for metacaspases), as well as metabolic (sphingolipid profiles) responses to the two triggers in the two cell lines. The role of NADPH oxidases and induction of transcripts for the class-II metacaspases MC5 differ qualitatively between the two cell lines. We tested a possible role of sphingolipid metabolism but can rule this out. We propose a model, where V. rupestris, originating from co-evolution with several biotrophic pathogens, readily activates a hypersensitive cell death in response to harpin, while the context of MeJA-induced cell death in 'Pinot Noir' might not be related to immunity at all. We propose that the underlying signalling is modular, recruiting metacaspases differently depending on upstream signalling.

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