TCP24 modulates secondary cell wall thickening and anther endothecium development.

Han Wang,Yuke He,Yanfei Mao,Jun Yang

doi:10.3389/fpls.2015.00436

Abstract

miR319-targeted TCP genes are believed to regulate cell division in leaves and floral organs. However, it remains unknown whether these genes are involved in cell wall development. Here, we report that TCP24 negatively regulates secondary wall thickening in floral organs and roots. The overexpression of the miR319a-resistant version of TCP24 in Arabidopsis disrupted the thickening of secondary cell walls in the anther endothecium, leading to male sterility because of arrested anther dehiscence and pollen release. Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants. By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening. Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.

Highlights

Anther dehiscence is a multistage process that involves coordinated programmed events in specific cells, including degeneration of the middle layer and the tapetum, thickening of the endothecium, degradation of septum cells, and breakage of stomium cells (Goldberg et al, 1993; Sanders et al, 1999; Wilson et al, 2011)
Other genes, such as CA2, AHP4 (Arabidopsis histidine-containing phosphotransfer factor 4), SAF1 and CBSX2, negatively regulate this process, and the overexpression of these genes in Arabidopsis leads to anther non-dehiscent phenotypes (Jung et al, 2008, 2013; Villarreal et al, 2009; Kim et al, 2012)
Overexpression of TCP24 Disrupts Anther Dehiscence in Arabidopsis Mutations in single CIN-like TCP genes do not generate visible phenotypes owing to the redundancy among these genes (Koyama et al, 2007)

Summary

Introduction

Anther dehiscence is a multistage process that involves coordinated programmed events in specific cells, including degeneration of the middle layer and the tapetum, thickening of the endothecium, degradation of septum cells, and breakage of stomium cells (Goldberg et al, 1993; Sanders et al, 1999; Wilson et al, 2011). Mutations in IRREGULAR XYLEM (IRX) and receptor-like protein kinase 2 (RPK2) genes lead to the defective secondary wall thickening of the anther (Brown et al, 2005; Mizuno et al, 2007; Hao et al, 2014) Other genes, such as CA2 (carbonic anhydrase 2), AHP4 (Arabidopsis histidine-containing phosphotransfer factor 4), SAF1 (secondary wall thickening-associated F-box 1) and CBSX2 (cystathionine β-synthase domain-containing protein), negatively regulate this process, and the overexpression of these genes in Arabidopsis leads to anther non-dehiscent phenotypes (Jung et al, 2008, 2013; Villarreal et al, 2009; Kim et al, 2012)

Methods

Results

Conclusion