Galactose-Depleted Xyloglucan Is Dysfunctional and Leads to Dwarfism in Arabidopsis. Issue 4 (11th February 2015)

• Record Type: Journal Article
• Authors: Kong, Yingzhen; Peña, Maria J.; Renna, Luciana; Avci, Utku; Pattathil, Sivakumar; Tuomivaara, Sami T.; Li, Xuemei; Reiter, Wolf-Dieter; Brandizzi, Federica; Hahn, Michael G.; Darvill, Alan G.; York, William S.; O'Neill, Malcolm A.
• Is Part Of: Plant physiology. Volume 167:Issue 4(2015)
• Page Start: 1296
• Page End: 1306
• Publication Date: 2015-02-11
• Subjects: Plant physiology -- Periodicals; Botany -- Periodicals; Periodicals; Electronic journals; 571.2
• DOI: 10.1104/pp.114.255943
• Languages: English
• ISSNs: 0032-0889

Abstract

Abstract : Depleting galactose from the cell wall polysaccharide xyloglucan leads to a disruption of diverse cellular and physiological processes involved in normal plant growth. Abstract: Xyloglucan is a polysaccharide that has important roles in the formation and function of the walls that surround growing land plant cells. Many of these plants synthesize xyloglucan that contains galactose in two different side chains (L and F), which exist in distinct molecular environments. However, little is known about the contribution of these side chains to xyloglucan function. Here, we show that Arabidopsis ( Arabidopsis thaliana ) mutants devoid of the F side chain galactosyltransferase MURUS3 (MUR3) form xyloglucan that lacks F side chains and contains much less galactosylated xylose than its wild-type counterpart. The galactose-depleted xyloglucan is dysfunctional, as it leads to mutants that are dwarfed with curled rosette leaves, short petioles, and short inflorescence stems. Moreover, cell wall matrix polysaccharides, including xyloglucan and pectin, are not properly secreted and instead accumulate within intracellular aggregates. Near-normal growth is restored by generating mur3 mutants that produce no detectable amounts of xyloglucan. Thus, cellular processes are affected more by the presence of the dysfunctional xyloglucan than by eliminating xyloglucan altogether. To identify structural features responsible for xyloglucan dysfunction, xyloglucan structure was modified in situ by generating mur3 mutants that lack specific xyloglucan xylosyltransferases (XXTs) or that overexpress the XYLOGLUCAN L-SIDE CHAIN GALACTOSYLTRANSFERASE2 ( XLT2 ) gene. Normal growth was restored in the mur3-3 mutant overexpressing XLT2 and in mur3-3 xxt double mutants when the dysfunctional xyloglucan was modified by doubling the amounts of galactosylated side chains. Our study assigns a role for galactosylation in normal xyloglucan function and demonstrates that altering xyloglucan side chain structure disturbs diverse cellular and physiological processes.