Abstract
Stress upregulates AGPs typified by gum exudates, a well-known wound stress response. Salt-stress also dramatically upregulates AGP release; recently we showed that four species, adapted to growth as suspension cultures in high salt, gave much higher AGP yields (mg AGP/g cells fresh weight) and AGP release rates than control cells. This discovery has wide ramifications. For example, quantifying the AGP flux through the cell surface pools [membrane-bound, soluble periplasmic, wall and growth medium (M → S → W → G[sink])] implied that AGPs migrate through the wall, mainly by ‘plug flow’ extrusion in rapidly growing unadapted tobacco BY-2 cells, but largely by diffusion in salt-adapted cells. We propose that AGPs may act as plasticizers by decreasing pectin cross-linking; this increases pectin porosity and enhances wall rheology. Thus we interpret the rapid inhibition of pollen tip growth by the Yariv reagent as a loss of monomeric AGP plasticizers when they form cross-linked Yariv-AGP complexes in muro.
Acknowledgements
This work was funded by grants from the National Science Foundation (MCB-9874744), the Herman Frasch Foundation (526-HF02) and the United States Department of Agriculture (2002-34490-11919) to M. J. K.; D. T. A. L. thanks The Royal Society for a travel grant and gratefully acknowledges the University of Sussex, School of Life Sciences and Professor Timothy Flowers for their laboratory facilities in the Plant Stress Unit, and thanks Prof. J-P. Joseleau, University of Joseph Fourier, Grenoble, France, for the Acacia senegal culture.
Notes
AGP, arabinogalactan-protein; AGM, arabinogalactan glycomodule; fw, fresh weight; GPI, glycosylphosphatidylinositol; Hyp, hydroxyproline; IPN, interpenetrating network; G, AGPs in the growth medium; M, plasma membrane-bound AGPs; S, soluble periplasmic AGPs; W, wall-bound AGPs; Td, total cell surface AGPs by direct assay of intact cells; Ti, total cell surface AGPs indirectly assayed in cell fractions