Abstract

Mutants affected in the Arabidopsis TBL29/ESK1 xylan O‐acetyltransferase display a strong reduction in total wall O‐acetylation accompanied by a dwarfed plant stature, collapsed xylem morphology, and enhanced freezing tolerance. A newly identified tbl29/esk1 suppressor mutation reduces the expression of the MAX4 gene, affecting the biosynthesis of methyl carlactonoate (MeCLA), an active strigolactone (SL). Genetic and biochemical evidence suggests that blocking the biosynthesis of this SL is sufficient to recover all developmental and stress‐related defects associated with the TBL29/ESK1 loss of function without affecting its direct effect—reduced wall O‐acetylation. Altered levels of the MAX4 SL biosynthetic gene, reduced branch number, and higher levels of MeCLA, were also found in tbl29/esk1 plants consistent with a constitutive activation of the SL pathway. These results suggest that the reduction in O‐acetyl substituents in xylan is not directly responsible for the observed tbl29/esk1 phenotypes. Alternatively, plants may perceive defects in the structure of wall polymers and/or wall architecture activating the SL hormonal pathway as a compensatory mechanism.

Highlights

  • The success of higher plants to colonize terrestrial habitats rests greatly upon the evolution of the vascular system, the xylem, a highly specialized tissue for conducting water, minerals, and nutrients from soil to leaves over long distances (Lucas et al, 2013)

  • Forward and reverse genetic approaches have indicated that a correct synthesis and/or coordinate deposition of the secondary wall components may be necessary for the proper formation of xylem cells and the functionality of the plant vascular system

  • The characteristic low wall acetylation content in tbl29 (42% reduction compared to wildtype) was retained in tbl29 max4-7 and tbl29 max4-1 plants (47% and 46% reduction, respectively), implying that xylan acetylation remains low in the tbl29-suppressed plants

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Summary

| INTRODUCTION

The success of higher plants to colonize terrestrial habitats rests greatly upon the evolution of the vascular system, the xylem, a highly specialized tissue for conducting water, minerals, and nutrients from soil to leaves over long distances (Lucas et al, 2013). Most of the irx mutants display structural alterations in the main polymer components of xylem secondary walls (i.e., cellulose, hemicelluloses, and/or lignin) and a concomitant collapse of the xylem cells resulting in a stunted growth phenotype and activation of stress responses. Replacing the acetyl-substitutents in the tbl mutant with glucuronic acid moieties through the expression of a glucuronic acid transferase lead to the abolishment of the irregular xylem phenotype and normal plant growth (Xiong, Dama, & Pauly, 2015; Mortimer et al, 2010). These data suggested that a properly acetylated xylan structure is required for proper xylem function. In this study, we describe a detailed characterization of a tbl suppressor mutant identified through a genetic suppressor screen uncoupling reduced xylan acetylation from the irregular xylem phenotype and providing evidence of an hitherto unreported role of the phytohormone strigolactone (SL) in the perception of secondary cell wall defects

| MATERIALS AND METHODS
| RESULTS
Findings
| DISCUSSION
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