Salt stress upregulates periplasmic arabinogalactan proteins: using salt stress to analyse AGP function*

Authors


  • *

    A preliminary account of this work was presented at the Xth International Cell Wall Meeting.

Author for correspondence: Derek T. A. Lamport Tel: +44 (0)1273 678715 Fax: +44 (0)1273 678937 Email: d.t.a.Lamport@sussex.ac.uk

Summary

  • • Arabinogalactan proteins (AGPs) are implicated in cell expansion by unknown mechanisms, thus AGP content and cell-expansion rate might be correlated.
  • • We used Yariv reagent to quantify release rates and distribution of AGP at the cell surface of tobacco BY-2 cells: plasma membrane (M); soluble periplasmic AGPs released by cell rupture (S); cell wall (W); and growth medium (Gsink).
  • • In contrast to earlier reports, we observed massive upregulation of AGPs in salt-stressed cells, and hence the absence of a simple, direct cause-and-effect relationship between growth rate and AGP release. There was a more subtle connection. A dynamic flux model, MSWGsink, indicated that turnover was nondegradative, with little free diffusion of AGPs trapped in the pectic matrix of nonadapted cells where transmural migration of high molecular-weight AGPs occurred mainly by plug flow (apposition and extrusion). In contrast, however, an up to sixfold increased AGP release rate in the slower-growing salt-adapted cells indicated a greatly increased rate of AGP diffusion through a much more highly porous pectic network.
  • • We hypothesize that classical AGPs act as pectin plasticizers. This explains how β-d-glycosyl Yariv reagents might inhibit expansion growth by crosslinking monomeric AGPs, and thus mimic an AGP loss-of-function mutation.

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