Discussion
In the current study, we provide evidence that remodelling of actin filaments (in our experiments induced by aluminium-dependent activation of the NADPH oxidase RboH) is sufficient to induce phytoalexins synthesis genes in grapevine. This activation of defence genes shares the dependence on MAPK signalling with flg22 triggered basal immunity, while being independent of calcium influx. The remodelling of actin is shared with cell-death related defence responses. However, this aluminium triggered defence response is not accompanied by cell death. Instead, aluminium also activates isochorismate synthase, a key enzyme for the synthesis of salicylic acid, as well as of PR1 , a gene which is known to be responsive to salicylic acid. In the following, we will discuss these findings in the context of a third defence pathway that bifurcates from cell-death related immunity (ETI) and merges into basal immunity (PTI), we will revisit the role of salicylic acid for basal immunity, and we will try to draw some conclusions on the nature and mechanisms of actin remodelling triggering this pathway, and give an outlook on potential applications for viticulture that can be derived from the current findings.