al. 1995). Touch-induced tendril coiling can be inhibited in this system by Gd3+and ery-
throsine B, a putative inhibitor of the Ca2+-ATPases that pump Ca2+into the ER. Thus,
there is some tentative evidence placing a Ca2+release channel involved in mechanore-
sponse on an intracellular membrane in this system. Interestingly, BCC1 may also be reg-
ulated by cytosolic pH and levels of reactive oxygen species (ROS) (Klusener et al.
1997). Considering the proposed roles for these two agents in response to mechanical
perturbation and gravistimulation (see below), BCC1 may be hinting at one mechanism
whereby gravity and touch signaling may modulate each other.
Although the link between touch and Ca2+is supported by a wealth of experimental
data, an equivalent connection between Ca2+and gravity signaling is less clear. There is
much circumstantial evidence linking Ca2+to the gravity response. For example, appli-
cation of Ca2+chelators such as EGTA and BAPTA abolishes the growth component of
the graviresponse (Lee et al. 1983a, 1983b; Björkman and Cleland 1991) and the auxin
fluxes that accompany tropic curvature (Young and Evans 1994; see also Chapter 3).
Similarly, a range of pharmacological agents thought to disrupt diverse aspects of Ca2+
signaling have been reported to alter gravitropism (Fasano et al. 2002; Massa et al. 2003).
There is also extensive evidence implicating the Ca2+-dependent regulatory protein
calmodulin (CaM) in the graviresponse. For example, CaM levels are enriched in the root
tip (the site of gravity perception) (Allan and Trewavas 1985; Stinemetz et al. 1987), are
enhanced upon gravistimulation (Sinclair et al. 1996), and the CaM levels in the root tip
correlate with the responsiveness of the organ to gravity (Stinemetz et al. 1987).
Calmodulin transcripts have also been shown to be recruited into polysomes on the lower
side of the gravistimualted pulvinus (Heilmann et al. 2001), suggesting that gravistimu-
lation should change the abundance of CaM across the stimulated organ. Calmodulin an-
tagonists inhibit the asymmetric Ca2+and proton fluxes associated with graviresponse
(Lee et al. 1983b, 1984; Björkman and Leopold 1987) and impair gravisensing and tropic
response at levels that do not inhibit growth (Stinemetz et al. 1992; Sinclair et al. 1996).
Although it is always important to view such pharmacological data with caution due to
unknown targets and side effects of the antagonists used, this body of data, taken with the
other evidence for a role for CaM described above, does point toward an important role
for this Ca2+-dependent protein in gravisignaling and response, and therefore, by impli-
cation, a role for Ca2+.
The identification of a possible role for inositol-1,4,5-trisphosphate (InsP 3 ) in grav-
isignaling/response is also consistent with Ca2+playing an important role in this process.
Classically, the activation of the phospholipids-cleaving enzyme phospholipase C is
thought to produce the second messengers diacylglycerol and InsP 3. The precise signal-
ing role for diacylglycerol in plants is still unclear but InsP 3 seems to play a similar role
to its function in animal cells in triggering signaling-related Ca2+release from intracel-
lular stores (Wang 2004). In the graviresponsive pulvinus from maize and oat, InsP 3 be-
comes elevated within minutes of gravistimulation, although a clear asymmetry in levels
between upper and lower side of the organ takes several minutes to appear (Perera et al.
1997, 1999, 2001). Phosphatidyl-inositol-phosphate (PIP) kinase activity similarly in-
creased, suggesting that levels of the substrate for phospholipase C (phosphatidylinositol-
4,5-bisphosphate) might be fuelling the elevated InsP 3 levels. Perera et al. (2006) showed
that InsP 3 also exhibits a three-fold increase within the first 15 minutes of gravsitmula-
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