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.