Auxin as an intercellular signal - Intercellular Communication in Plants - page 11

crucial question remains of what the biological relevance of the PIN cycling is. Here
different scenarios can be conceived:
1. A high turnover of PAT components would provide the flexibility to allow
rapid changes in polarity of carrier distribution and provide a mechanism
for the rapid redirection of auxin fluxes in response to environmental or
developmental cues (Friml & Palme, 2002). Indeed, PIN3 was shown to
rapidly relocate in response to gravity stimulation (Plate 1.1M) (Friml et al .,
2002a).
2. Components of polar auxin transport may have a dual receptor/transporter
function (Hertel, 1983). In this case, cycling may be part of a mechanism
for signal transduction and receptor regeneration, as is known for some
other kinds of receptors. Dual sensor and transport functions have been
proposed for sugar transporters in yeast and plants (Lalonde et al ., 1999).
3. The most exciting possibility is that vesicle trafficking itself is a part of
the PAT mechanism and that, in a manner analogous to the mechanism of
neurotransmitter release in animals, auxin is a vesicle cargo, released from
cells by polar exocytosis (Friml & Palme, 2002). In this model, instead
of being 'auxin channels', PIN proteins would mediate the accumulation
or retention of auxin in the vesicles in which auxin would be translo-
cated. Some support of this scenario comes from the BIG protein, which
is involved in PAT and PIN1 subcellular trafficking, since its homolog in
Drosophila mediates vesicle recycling during synaptic transmission.
Regardless of how well any of the scenarios described above eventually turns out
to fit the true picture, an understanding of the cellular mechanisms controlling the
subcellular dynamics of the auxin carriers will be crucial for our understanding of
PAT process.
1.4.2 AEIs and vesicle trafficking
Another surprising outcome of the cell-biological studies on PIN cycling concerns
effects of AEIs such as TIBA on vesicle trafficking (Fig. 1.4). Despite the fact
that AEIs were major tools for physiological studies on PAT, the mechanism of their
action remains elusive. The finding that TIBA inhibits PIN1 recycling (Geldner et al .,
2001) raised an attractive possibility that TIBA inhibits auxin efflux by interfering
with the recycling of auxin efflux components. However, AEIs also interfere with
vesicle-mediated traffic of PAT unrelated proteins and much higher concentrations
are needed for trafficking inhibition than for PAT inhibition. In addition, observations
on BY-2 tobacco cells have revealed that the inhibition of auxin efflux by NPA is
much more efficient than the inhibition caused by the well-established inhibitor of
protein traffic BFA (Petrasek et al ., 2003). These findings argue against a causal
link between a general role of NPA and other phytotropins in vesicle trafficking
and auxin efflux inhibition. Thus, it still remains open whether inhibition of vesicle
traffic and PAT by AEIs are functionally related.