Aluminum-induced 1 -> 3-beta-D-glucan inhibits cell-to-cell trafficking ofmolecules through plasmodesmata. A new mechanism of aluminum toxicity in plants
M. Sivaguru et al., Aluminum-induced 1 -> 3-beta-D-glucan inhibits cell-to-cell trafficking ofmolecules through plasmodesmata. A new mechanism of aluminum toxicity in plants, PLANT PHYSL, 124(3), 2000, pp. 991-1005
Symplastic intercellular transport in plants is achieved by plasmodesmata (
PD). These cytoplasmic channels are well known to interconnect plant cells
to facilitate intercellular movement of water, nutrients, and signaling mol
ecules including hormones. However, it is not known whether Al may affect t
his cell-to-cell transport process, which is a critical feature for roots a
s organs of nutrient/water uptake. We have microinjected the dye lucifer ye
llow carbohydrazide into peripheral root cells of an Al-sensitive wheat (Tr
iticum aestivum cv Scout 66) either before or after Al treatment and follow
ed the cell-to-cell dye-coupling through PD. Here we show that the Al-induc
ed root growth inhibition is closely associated with the Al-induced blockag
e of cell-to-cell dye coupling. Immunofluorescence combined with immune-ele
ctron microscopic techniques using monoclonal antibodies against 1-->3-beta
-D-glucan (callose) revealed circumstantial evidence that Al-induced callo
se deposition at PD may responsible for this blockage of symplastic transpo
rt. Use of 2-deoxy-D-glucose, a callose synthesis inhibitor, allowed us to
demonstrate that a reduction in callose particles correlated well with the
improved dye-coupling and reduced root growth inhibition. While assessing t
he tissue specificity of this Al effect, comparable responses were obtained
From the dye-coupling pattern in tobacco (Nicotiana tabacum) mesophyll cel
ls. Analyses of the Al-induced expression of PD-associated proteins, such a
s calreticulin and unconventional myosin VIII, showed enhanced fluorescence
and co-localizations with callose deposits. These results suggest that Al-
signal mediated localized alterations to calcium homeostasis may drive call
ose formation and PD closure. Our data demonstrate that extracellular Al-in
duced callose deposition at PD could effectively block symplastic transport
and communication in higher plants.