cally stimulated, the motility of the sedimenting statoliths is reduced (Massa and Gilroy
2003a). This reduced motility would provide a system whereby touch stimulation could
reduce gravitropic response by simply reducing the sedimentation rate to the gravity re-
sponsive component of the sensory cell. However, it appears that such a model of sens-
ing based on large-scale amyloplast sedimentation may be too simplistic a view of these
initial sensory events. Thus, perception and presentation times (measures of the time to
generate and export the initial gravitropic signal) fall in the seconds to < 1 minute range,
times much less than required for amyloplasts in the sensory cells to completely sediment
to the new, lower face (Hejnowicz et al. 1998; Perbal et al. 2002; Perbal and Driss-Ecole
2003). Such rapid generation of signal implies that the amyloplasts are in contact with
some network that rapidly converts the force of their sedimentation to a biochemical sig-
nal. The cytoskeleton remains a prime candidate for such a network in most gravisensing
models (Blancaflor 2002; see also Chapters 1 and 2).
Filamentous actin in particular has been proposed to play a critical role in gravisensi-
tivity, based on its abundant presence in columella cells (Yoder et al. 2001; Blancaflor
2002). The “restrained gravisensing” model (Baluˇska and Hasenstein 1997; Hejnowicz
et al. 1998; Driss-Ecole et al. 2000; Perbal et al. 2002) suggests that amyloplasts are
physically connected to the actin network, which then in turn connects to downstream
components of the signaling cascade. Alternatively, in unrestrained gravity sensing, any
connections between the cytoskeleton and the statoliths are nonexistent, too weak, or
too transient to provide direct mechanotransduction. In this model, the dense actin web
in a columella cell is deformed locally by sedimenting amyloplasts, resulting in distant
effects in the cell such as activation or inactivation of mechanoreceptors on the plasma
membrane.
The reduced amyloplast motility induced by mechanical stimulation would therefore
deliver less force to the actin network and so reduce gravitropic signal generation. Recent
data suggest that this view of the role of actin may also be too simple. For example, dis-
rupting the actin network (Blancaflor and Hasenstein 1997; Staves et al. 1997a) does not
block the gravitropic response but, rather, enhances organ bending (Blancaflor and
Hasenstein 1997; Yamamoto and Kiss 2002; Blancaflor and Masson 2003; Hou et al.
2003; Hou et al. 2004), suggesting that actin may operate to down-regulate gravitropic
signaling. In this case mechanostimulation may actually be enhancing the interactions of
actin with statoliths to inhibit gravitropic response.
The graviresponse is also accompanied by an immediate cytoplasmic pH increase after
reorientation that is required for maximal gravitropic bending (Scott and Allen 1999;
Fasano et al. 2001). This pH increase is extended by treatments which disrupt actin fila-
ments (Hou et al. 2004). It is possible that actin regulates transport processes at the
plasma membrane, leading to the down-regulation of the pH signal, facilitating a reset-
ting of the gravitropic signaling system (Hou et al. 2004). The pH change itself should
have far-reaching effects in the cell, as a change in pH will alter the activity of most pro-
teins in the cytoplasm. Thus, pH changes may represent a way to effect a large-scale
change of cell activities upon gravistimulation, and touch may be acting through actin to
modulate this system.
The gravity-related pH changes may also alter auxin distribution by changing the
chemiosmotic driving force for auxin uptake/redistribution into the columella (Friml et
frankie
(Frankie)
#1