The histone deacetylase HDA19 controls root cell elongation and modulates a subset of phosphate starvation responses in Arabidopsis.

Chun-Ying Chen,Wolfgang Schmidt,Keqiang Wu

doi:10.1038/srep15708

Abstract

The length of root epidermal cells and their patterning into files of hair-bearing and non-hair cells are genetically determined but respond with high plasticity to environmental cues. Limited phyto-availability of the essential mineral nutrient phosphate (Pi) increases the number of root hairs by longitudinal shortening of epidermal cells and by reprogramming the fate of cells in positions normally occupied by non-hair cells. Through analysis of the root morphology and transcriptional profiles from transgenic Arabidopsis lines with altered expression of the histone deacetylase HDA19, we show that in an intricate interplay of Pi availability and intrinsic factors, HDA19 controls the epidermal cell length, probably by altering the positional bias that dictates epidermal patterning. In addition, HDA19 regulates several Pi-responsive genes that encode proteins with important regulatory or metabolic roles in the acclimation to Pi deficiency. In particular, HDA19 affects genes encoding SPX (SYG1/Pho81/XPR) domain-containing proteins and genes involved in membrane lipid remodeling, a key response to Pi starvation that increases the free Pi in plants. Our data add a novel, non-transcriptionally regulated component of the Pi signaling network and emphasize the importance of reversible post-translational histone modification for the integration of external signals into intrinsic developmental and metabolic programs.

Highlights

The length of root epidermal cells and their patterning into files of hair-bearing and non-hair cells are genetically determined but respond with high plasticity to environmental cues
We report that HDA19 controls several responses to Pi starvation, including root hair density, epidermal cell elongation and membrane lipid remodeling, thereby accentuating the critical involvement of chromatin modifications in phenotypic plasticity
To investigate whether reversible histone acetylation is important for the Pi deficiency-induced root hair phenotype, we tested homozygous mutants or knock-down lines defective in the expression of HDA18, HDA17, an unclassified member of the RPD3-like superfamily, and the class I members HDA6, HDA9 and HDA19 for their root hair phenotypes under control and low Pi conditions

Summary

Introduction

The length of root epidermal cells and their patterning into files of hair-bearing and non-hair cells are genetically determined but respond with high plasticity to environmental cues. The activator complex induces the expression of the R3 MYB transcription factor CPC, a positive regulator of the hair fate, which migrates via plasmodesmata to hair cells where it competes with WER for binding to the activator complex[9]. The higher root hair frequency of Pi-deficient plants results from reduced longitudinal elongation of epidermal cells and additional hair fate assignment of N-positioned cells[11]. This response has been explored for the widely used Columbia (Col-0) strain, but large variations appear to exist across Arabidopsis accessions[12]. Alterations in the activity of HDA18 lead cells in N positions to adopt the hair cell fate[20,21]

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Conclusion