The plant cytoskeleton is a network of dynamic filamentous proteins that consist of
microtubules, actin filaments (F-actin), and a number of accessory proteins (Blancaflor
et al. 2006). In the mid- to late 1980s, interest in the cytoskeleton as a mediator of plant
gravity sensing was ignited when Wolfgang Hensel published a series of papers describ-
ing the organization of the cytoskeleton in the root columella in an attempt to explain the
highly polarized nature of this particular cell type (Hensel 1985, 1988, 1989). This was
followed by a series of studies on the structure of the cytoskeleton in gravity-sensing cells
of roots and shoots, which continued for several years (e.g., White and Sack 1990;
Baluˇska et al. 1997; Collings et al. 1998; Collings et al. 2001; Driss-Ecole et al. 2000);
(Figure 1.2).
The widespread interest in describing the nature of the cytoskeleton in statocytes was
likely triggered by the proposal of Andreas Sievers and colleagues in the late 1980s that
the cytoskeleton may not only be involved in maintaining statocyte polarity but could also
be a direct cellular target of sedimenting amyloplasts, raising the possibility that it might
function as a gravity receptor. Sievers et al. (1991) suggested that sedimenting amylo-
plasts could pull on the cytoskeleton, particularly on F-actin networks, triggering a cas-
cade of signaling events leading to differential organ growth. Indeed, this proposal has
been supported by several studies demonstrating that amyloplast movement is dependent
on the actin cytoskeleton since drugs that disrupt F-actin alter the dynamics and sedimen-
tation of amyloplasts in space (Volkmann et al. 1999) and on the ground (Hou et al. 2004;
Saito et al. 2005; Palmieri and Kiss 2005). In shoot endodermal cells, for example, amy-
loplast position is restricted by the large, centrally located vacuole, and amyloplasts have
to traverse the thin cytoplasmic strands within the cell to sediment (Kato et al. 2002; Saito
et al. 2005).
As noted earlier, mutants impaired in shoot gravitropism have defects in vacuolar
membrane dynamics, and it is possible that the cytoskeleton may function in shoot grav-
ity sensing by regulating the trafficking of vesicles to the vacuole and indirectly influenc-
ing amyloplast sedimentation (Morita et al. 2002; Yano et al. 2003). Indeed, shoots treated
with latrunculin B, a drug that disrupts F-actin, showed reduced amyloplast settling upon
gravistimulation (Friedman et al. 2003; Palmieri and Kiss 2005; Saito et al. 2005). One
would predict that if amyloplast sedimentation was impeded by F-actin disruption, the
ability of shoots to bend after a gravity stimulus would be inhibited due to altered grav-
ity sensing. Although one study in snapdragon inflorescence stems has demonstrated that
this is indeed the case (Friedman et al. 2003), a number of other reports surprisingly show
that altering the actin cytoskeleton with latrunculin B can actually promote gravitropism
in shoots (Yamamoto and Kiss 2002; Palmieri and Kiss 2005; Saito et al. 2005).
It is difficult to explain how impeding the mass translocation of amyloplasts in shoots
by disrupting F-actin can promote gravitropism, considering the predictions of the starch-
statolith hypothesis. However, one way to interpret these recent results is to view the
actin-dependent saltatory movement of amyloplasts in the statocytes as background
noise. Reduction of this noise by latrunculin B would essentially increase system sensi-
tivity leading to enhanced gravitropism. Although a majority of amyloplasts in the endo-
dermis are rendered immobile after latrunculin B treatment (Palmieri and Kiss 2005), the
few “rogue” amyloplasts that still manage to sediment could still be sufficient to trigger
a gravity signal (Saito et al. 2005). With the diminished background noise, the signal gen-
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