Abstract

The root growth of most crop plants is inhibited by soil salinity. Roots respond by modulating metabolism, gene expression and protein activity, which results in changes in cell wall composition, transport processes, cell size and shape, and root architecture. Here, we focus on the effects of salt stress on cell wall modifying enzymes, cellulose microfibril orientation and non-cellulosic polysaccharide deposition in root elongation zones, as important determinants of inhibition of root elongation, and highlight cell wall changes linked to tolerance to salt stressed and water limited roots. Salt stress induces changes in the wall composition of specific root cell types, including the increased deposition of lignin and suberin in endodermal and exodermal cells. These changes can benefit the plant by preventing water loss and altering ion transport pathways. We suggest that binding of Na+ ions to cell wall components might influence the passage of Na+ and that Na+ can influence the binding of other ions and hinder the function of pectin during cell growth. Naturally occurring differences in cell wall structure may provide new resources for breeding crops that are more salt tolerant.

Introduction

Plant evolution has resulted in a large array of mechanisms to tolerate the stresses associated with increased soil salinity. However, for most cereal crops the growth of roots is disrupted when soil salinity exceeds 4 dS/m, equivalent to about 40 mM NaCl. Increased soil salinity exposes plants to ionic sodium (Na+) and chloride (Cl−), which leads to a cascade of responses in the plant due to the ionic and osmotic components of salt stress [1,2].

Salt stress can indirectly affect cell wall properties by causing changes in gene expression, but Na+ can also physically interact with the cell wall components directly, and change their chemical properties [3]. An increase in soil salinity results in accumulation of Na+ in the apoplast, which can lead to an increase in interactions between Na+ and negatively charged sites within cell wall polymers, and also influence apoplastic pH. Salinity causes transient alkalinisation of the apoplast, and this could limit growth in the context of the acid growth theory [4,5]: Auxin activates plasma membrane H+-ATPases and protons are extruded into the apoplast, apoplastic acidification induces cell wall loosening by activating expansins and other remodelling enzymes resulting in loosening of the cell wall. Hence, growth could be limited by a decrease in free apoplastic protons causing a shift in the apoplastic pH away from the range that favors cell-wall loosening [4], although in maize the inhibition of growth as a result of salinity was not associated with the capacity of the epidermal cells to acidify their walls [6].