Defence-related actin remodeling can be separated from
defence-related cell-death
Actin remodelling has been recognised as early event heralding ensuing
programmed cell death (reviewed in Gourlay & Ayscough, 2005;
Franklin-Tong & Gourlay, 2008; Smertenko & Franklin-Tong, 2011). In
grapevine cells, as well, the induction of programmed cell death, by
either the bacterial elicitor harpin (Chang et al. , 2015; Qiao et
al. , 2010), the stilbene aglycone resveratrol (Chang et
al. , 2011), or the oxylipin derivative 3-cis -hexenal
(Akaberi et al. , 2018) were preceded by actin remodelling,
involving a depletion of the fine subcortical meshwork and massive
bundling of transvacuolar actin cables. Thus, in these cases, actin
remodelling was tightly correlated with programmed cell death. A
correlation of two events is a necessary condition for claiming a causal
relation between these two events. However, even if this correlation is
tight, it cannot be considered as sufficient for causality.
In fact, actin remodelling of a similar type can be observed without any
correlation with cell death. For instance, depletion of cortical actin
and condensation of actin cables have been also observed in response to
auxin depletion (Waller et al. , 2002), or in response to
activation of the plant photoreceptor phytochrome (Waller & Nick,
1997), both events that occur in the absence of any cell death.
The same conclusion is reached by our observation that aluminium did not
cause any significant increase of mortality (Suppl. Figure S4 ).
Is actin remodelling just a side phenomenon, then? This seems not to be
the case either, because in the same cell system (V. rupestris ),
the induction of programmed cell death by harpin had been shown to be
significantly mitigated by pretreatment with Latrunculin B (Chang et
al. , 2015), which provides evidence that actin is necessary to
activate cell death.
Thus, while actin remodelling is, usually, accompanied by
defence-related cell death, and while suppression of actin remodelling
will impair defence-related cell death, this apparently tight link is
uncoupled in case of aluminium treatment. The most straightforward
explanation would be that actin remodelling has to coincide with a
second signal to activate programmed cell death. This second signal
cannot be the apoplastic oxidative burst generated by RboH, because
aluminium does trigger this response (Achary et al. , 2012).
Moreover, we observed that actin remodelling in response to aluminium
can be suppressed by diphenylene iodonium, indicative of RboH activity
as transducing event (Figure 2 ). While in case of a real
pathogen attack apoplastic oxidative burst is accompanied by calcium
influx, this does not seem to be the case for aluminium (Suppl.
Figure S3 ). A parsimonious hypothesis would therefore assume that
calcium influx as a second signal is required to activate programmed
cell death.