References

21 Wounding, electrical signals, the cytoskeleton, and gene expression 311
ron’s length. This prevents the tissue through which it is passing being
“informed”, and also speeds up the rate of transmission by having the
signal (ion flux, change in membrane potential) jump from “leak-point”
to “leak-point.” In contrast, APs in plants and in nonneuronal tissues can
be thought of as megaphones, where signal velocity is reduced in order to
maximize information spread, i.e., all the cells on the pathway (especially
the phloem) are informed, and presumably modified, by the passing signal
(Davies 1987a, 1987b; Zawadzki et al. 1991).
The VP differs considerably from the AP; it is not all-or-nothing, nor is
it self-perpetuating (Stankovic et al. 1997c), rather it is a hydraulic surge,
or possibly a transported chemical (Malone 1996) in the xylem evoking
local changes in membrane potential in adjacent living cells. The rapid loss
of tension in (dead) xylem elements is transduced into local changes in
ion flux through mechano-sensory ion channels in the adjacent living cells
(Stankovic et al. 1997b,c, 1998) or perhaps via ligand-activated channels if
there is a chemical transported (Malone 1996). Thus, continuing with the
information transmission analogy, the VP could be likened unto a radio
signal being broadcast throughout the plant and “heard” on all the cells in
the vicinity.
Regardless of the exact mechanism of transmission of APs and VPs,
the responses they evoke must depend on either the ions traversing the
membraneorthechangeinmembranepotential,orboth.Evidencesuggests
that both signals might involve calcium influx followed by chloride
and potassium efflux. However, even if the same ions are involved, the
downstream events might not be the same, since the flux of any ion will
depend on the kind, location, number, connections, and other properties
of the channel through which it passes. For instance, voltage-gated
calcium channels involved in APs might open only transiently, be few in
number, be located primarily in the phloem along the longitudinal axis
and be connected to the microtubules (Thuleau et al. 1998), where they
can interact with microtubule-associated Ca-binding proteins. In contrast,
mechano-sensitive calcium channels involved in VPs might be open for
longer periods, be abundant, be located primarily in living cells adjacent
to the xylem around the entire cell and be connected to the microfilaments
where they can interact with microfilament-associated Ca-binding proteins
(Davies 1993; Wang et al. 2004). Finally, voltage-gated, mechano-sensitive,
and especially ligand-activated calcium channels are likely to release some
calcium into the soluble phase in the vicinity of the plasma membrane,
where they can activate enzymes such as phospholipase C which will release
another second messenger, IP3, from membranes, which, in turn,
causes the release of more calcium from internal stores (Heilmann et al.
2001).