Abstract

Cell-to-cell adhesion in plants is mediated by the cell wall and the presence of a pectin-rich middle lamella. However, we know very little about how the plant actually controls and maintains cell adhesion during growth and development and how it deals with the dynamic cell wall remodeling that takes place. Here we investigate the molecular mechanisms that control cell adhesion in plants. We carried out a genetic suppressor screen and a genetic analysis of cell adhesion-defective Arabidopsis thaliana mutants. We identified a genetic suppressor of a cell adhesion defect affecting a putative O-fucosyltransferase. Furthermore, we show that the state of cell adhesion is not directly linked with pectin content in the cell wall but instead is associated with altered pectin-related signaling. Our results suggest that cell adhesion is under the control of a feedback signal from the state of the pectin in the cell wall. Such a mechanism could be necessary for the control and maintenance of cell adhesion during growth and development.

Highlights

  • Cell-to-cell adhesion in plants is established during cell division by the formation of a new cell wall between two daughter cells (Jarvis et al, 2003)

  • A deficiency in pectin synthesis was previously shown to lead to a loss of cell adhesion (Bouton et al, 2002; Mouille et al, 2007)

  • Mutations in QUASIMODO1 (GAUT8) and QUASIMODO2 (TSD2, OSU1), which respectively encode a putative galacturonosyltransferase of the GT8 family of glycosyltransferases and a putative pectin methyltransferase, lead to a 50% reduction in homogalacturonan (HG; the main component of the pectins) content, and a clear cell

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Summary

Introduction

Cell-to-cell adhesion in plants is established during cell division by the formation of a new cell wall between two daughter cells (Jarvis et al, 2003). Its constant synthesis and remodeling mediate the growth and development of the plant, and feedback signals concerning the integrity of the cell wall provide vital cues for the plant (Wolf et al, 2012a). A deficiency in pectin synthesis was previously shown to lead to a loss of cell adhesion (Bouton et al, 2002; Mouille et al, 2007). Mutations in QUASIMODO1 (GAUT8) and QUASIMODO2 (TSD2, OSU1), which respectively encode a putative galacturonosyltransferase of the GT8 family of glycosyltransferases (www.cazy.org) and a putative pectin methyltransferase, lead to a 50% reduction in homogalacturonan (HG; the main component of the pectins) content, and a clear cell-

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