Abstract
Root development is regulated by the tripeptide glutathione (GSH), a strong non-enzymatic antioxidant found in plants but with a poorly understood function in roots. Here, Arabidopsis mutants deficient in GSH biosynthesis (cad2, rax1, and rml1) and plants treated with the GSH biosynthesis inhibitor buthionine sulfoximine (BSO) showed root growth inhibition, significant alterations in the root apical meristem (RAM) structure (length and cell division), and defects in lateral root formation. Investigation of the molecular mechanisms of GSH action showed that GSH deficiency modulated total ubiquitination of proteins and inhibited the auxin-related, ubiquitination-dependent degradation of Aux/IAA proteins and the transcriptional activation of early auxin-responsive genes. However, the DR5 auxin transcriptional response differed in root apical meristem (RAM) and pericycle cells. The RAM DR5 signal was increased due to the up-regulation of the auxin biosynthesis TAA1 protein and down-regulation of PIN4 and PIN2, which can act as auxin sinks in the root tip. The transcription auxin response (the DR5 signal and expression of auxin responsive genes) in isolated roots, induced by a low (0.1 µM) auxin concentration, was blocked following GSH depletion of the roots by BSO treatment. A higher auxin concentration (0.5 µM) offset this GSH deficiency effect on DR5 expression, indicating that GSH deficiency does not completely block the transcriptional auxin response, but decreases its sensitivity. The ROS regulation of GSH, the active GSH role in cell proliferation, and GSH cross-talk with auxin assume a potential role for GSH in the modulation of root architecture under stress conditions.
Highlights
The continuous adjustment of phenotypic responses is a vital component of the process of plant adaptation to specific growth conditions and involves the coordinated activation of multiple cellular sensors and signalling pathways (Potters et al, 2007, 2009) [1,2]
In root apical meristem (RAM), we studied the effect of GSH on the expression and localization of PIN proteins and on the expression of the TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS1 (TAA1) auxin biosynthesis protein
We evaluated the effect of GSH on the root apical meristem (RAM) and on the growth of primary roots by analyzing the GSH-deficient mutants of the γ-EC synthase gene (At4g23100)
Summary
The continuous adjustment of phenotypic responses is a vital component of the process of plant adaptation to specific growth conditions and involves the coordinated activation of multiple cellular sensors and signalling pathways (Potters et al, 2007, 2009) [1,2]. GSH is a ubiquitous tripeptide that takes part in transducing environmental signals and plays a key role in plant responses to abiotic stress [3]. GSH possesses a cysteine thiol group that serves as a proton donor; GSH can undergo reversible oxidation to form glutathione di-sulfide (GSSG), which, in turn, can be reduced back to GSH through the activity of glutathione reductase (GR) This alternation of glutathione redox states contributes to the maintenance of the redox balance of ascorbate (ASC) or glutaredoxin/thioredoxin (reviewed in [4,5,6,7]). Cells in non-stress conditions have a high GSH/GSSG (2GSH) ratio, which is maintained through de novo GSH synthesis, enzymatic reduction of GSSG by GR, and uptake of exogenous GSH [8]
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