Project description:The balance between cell proliferation, differentiation and elongation rates emerges from gene regulatory networks coupled to various signal transduction pathways, including reactive oxygen species (ROS) and transcription factors, to respond to environmental cues. The Arabidopsis thaliana primary root has become a valuable system to unravel such networks and the role of transcription factors mediating the inhibition of primary root growth by ROS is just beginning to be studied. In this study, we demonstrate that the MADS-box transcription factor XAANTAL1 (XAL1) mediates the role of hydrogen peroxide (H2O2) in primary root growth and root stem cell niche identity. Interestingly, our findings suggest that XAL1 acts as a positive regulator of H2O2 concentration in the root meristem by directly regulating genes involved in oxidative stress response, such as PEROXIDASE 28 (PER28). Moreover, we found that XAL1 is necessary for the H2O2-induced inhibition of primary root growth through the negative regulation of peroxidase and catalase activities. Furthermore, we found that XAL1 together with RETINOBLASTOMA-RELATED (RBR), is also necessary to positively regulate the differentiation of columella stem cells triggered by a moderate oxidative stress induced by H2O2 treatment.
Project description:As a signal molecular in aerobic organism, how reactive oxygen species (ROS) regulates normal life is a fundamental biological question. Locally accumulated ROS have been reported to balance cell division and differentiation in root apical meristem. However, the underlying molecular mechanism is unclear. Here, we reveal that developmentally produced H2O2 in plant root apical meristem (RAM) triggers reversible acetylation modification of proteins which involved in protein synthesis and cell proliferation. WOX11, an essential transcription factor for crown roots (CRs) formation, modulates ROS homeostasis by directly regulating class III peroxidases. HDACs (histone deacetylases) sense cellular redox status to enhance their enzyme activities, which drives protein acetylation level alterations in rice roots. Oxidation-dependent on WOX11 triggered protein acetylation modification leads to a robust root system in rice. Our study revealed a novel regulatory mechanism which cellular redox status via a WOX11-dependent manner regulates protein acetylation during rice crown root development. The molecular link between the redox status and HDACs activities through WOX11-dependent pathway may provide new insight into which plants exploit developmentally produced ROS to direct organogenesis. Additionally, HDACs reversible enzyme activity via redox-regulated endows with the flexibility of protein modification control in dealing with developmental and changing environmental cues.
Project description:Plants reorganize their root architecture to avoid growth into unfavorable regions of the rhizosphere. In a screen based on chimeric repressor gene-silencing technology, we identified the Arabidopsis thaliana GeBP-LIKE 4 (GPL4) transcription factor as an inhibitor of root growth that is induced rapidly in root tips in response to cadmium (Cd). We tested the hypothesis that GPL4 functions in the root avoidance of Cd by analyzing root proliferation in split medium, in which only half of the medium contained toxic concentrations of Cd. The wild-type (WT) plants exhibited root avoidance by inhibiting root growth in the Cd side but increasing root biomass in the control side. By contrast, GPL4-suppression lines exhibited nearly comparable root growth in the Cd and control sides and accumulated more Cd in the shoots than did the WT. GPL4 suppression also altered the root avoidance of toxic concentrations of other essential metals, modulated the expression of many genes related to oxidative stress, and consistently decreased reactive oxygen species concentrations. We suggest that GPL4 inhibits the growth of roots exposed to toxic metals by modulating reactive oxygen species concentrations, thereby allowing roots to colonize noncontaminated regions of the rhizosphere.thereby re-allocating root biomass toward non-contaminated rhizosphere areas and minimizing root exposure to toxic metals.
Project description:Phosphate is an essential macronutrient required for plant growth and development. However, it is present at suboptimal levels in many terrestrial ecosystems. To ameliorate this limitation, plants have evolved developmental and physiological mechanisms known as phosphate starvation responses (PSR). One of the main PSR in Arabidopsis thaliana is a deep restructuration of the root system architecture, which includes a reduction in primary root growth resulting in a shallower root system better adapted to explore the nutrient-rich topsoil. Intense research over the last years has shown that this developmental change is dependent on the accumulation and redistribution of iron (Fe) at the root tip, which in turn, participates in Fenton reactions and generates reactive oxygen species that affect meristem function and cell elongation. We have recently identified and characterized a cytochrome-containing protein in A. thaliana, named CRR, which is involved in the primary root growth response to phosphate starvation. Our results showed that CRR is an ascorbate-dependent ferric-reductase whose expression levels modulates iron distribution pattern in the root, affecting meristem function and cell elongation. Moreover, this activity also has shown to be critical for iron toxicity tolerance since CRR determines the transport rate of iron from root to shoot.
Project description:Phosphate is an essential macronutrient required for plant growth and development. However, it is present at suboptimal levels in many terrestrial ecosystems. To ameliorate this limitation, plants have evolved developmental and physiological mechanisms known as phosphate starvation responses (PSR). One of the main PSR in Arabidopsis thaliana is a deep restructuration of the root system architecture, which includes a reduction in primary root growth resulting in a shallower root system better adapted to explore the nutrient-rich topsoil. Intense research over the last years has shown that this developmental change is dependent on the accumulation and redistribution of iron (Fe) at the root tip, which in turn, participates in Fenton reactions and generates reactive oxygen species that affect meristem function and cell elongation. We have recently identified and characterized a cytochrome-containing protein in A. thaliana, named CRR, which is involved in the primary root growth response to phosphate starvation. Our results showed that CRR is an ascorbate-dependent ferric-reductase whose expression levels modulates iron distribution pattern in the root, affecting meristem function and cell elongation. Moreover, this activity also has shown to be critical for iron toxicity tolerance since CRR determines the transport rate of iron from root to shoot.
Project description:Purpose: Although five receptors of RGF1 have recently been identified, the downstream signaling mechanism remains unknown. The goal of this study is to elucidate signaling events following RGF1 action. Methods: mRNA profiles of the root meristematic zone from Arabidopsis seedlings with or without RGF1 treatment were generated by deep sequencing, in triplicate. The sequence reads were analyzed using Tophat and DESeq2. The mutants of selected differentially expressed genes were generated for phenotyping. Results: Our study uncovered a series of signaling events following RGF1 action. The RGF1-receptor pathway controls distribution of reactive oxygen species (ROS) along the developmental zones of the Arabidopsis root. We identify a novel transcription factor, RGF1 INDUCIBLE TRANSCRIPTION FACTOR 1 (RITF1), which plays a central role in mediating RGF1 signaling. Manipulating RITF1 expression leads to redistribution of ROS along the root developmental zones. Changes in ROS distribution, in turn, enhance the stability of the PLETHORA2 (PLT2) protein, a master regulator of root stem cells. Conclusions: Our study clearly depicts a signaling cascade initiated by RGF1 and links the RGF1 peptide to ROS regulatory mechanisms.
Project description:We report the discovery of a root growth program in Arabidopsis that is independent of a functional quiescent center (QC). In this regulatory program, PHABULOSA (PHB), posttranscriptionally regulated by SHR and SCR, plays a central role. In phb shr and phb scr mutants, root meristem/growth activity recovers significantly. Interestingly, this recovery does not accompany the resurgence of QC cells. PHB regulates apical root growth in stele cells of the root meristem, located proximal to the QC. Our genome-wide investigation suggests that PHB exerts its influence on root growth by regulating auxin-cytokinin homeostasis. Apical root growth was restored when cytokinin levels were genetically reduced in the shr mutant. Conversely, when miRNA-resistant PHB was expressed in the root stele cells, apical root growth and meristem functions were significantly inhibited without blocking the QC identity. Taken together, our investigation reveals two mechanisms through which SHR regulates root growth and stem cell activities: one is to specify and maintain the QC and the other is to regulate the proximal meristem activity through PHB and cytokinin. In this regulation, QC seems to be more involved in maintaining the “growth signal” and thus ensure the indeterminate root growth.
Project description:We report the discovery of a root growth program in Arabidopsis that is independent of a functional quiescent center (QC). In this regulatory program, PHABULOSA (PHB), posttranscriptionally regulated by SHR and SCR, plays a central role. In phb shr and phb scr mutants, root meristem/growth activity recovers significantly. Interestingly, this recovery does not accompany the resurgence of QC cells. PHB regulates apical root growth in stele cells of the root meristem, located proximal to the QC. Our genome-wide investigation suggests that PHB exerts its influence on root growth by regulating auxin-cytokinin homeostasis. Apical root growth was restored when cytokinin levels were genetically reduced in the shr mutant. Conversely, when miRNA-resistant PHB was expressed in the root stele cells, apical root growth and meristem functions were significantly inhibited without blocking the QC identity. Taken together, our investigation reveals two mechanisms through which SHR regulates root growth and stem cell activities: one is to specify and maintain the QC and the other is to regulate the proximal meristem activity through PHB and cytokinin. In this regulation, QC seems to be more involved in maintaining the M-bM-^@M-^\growth signalM-bM-^@M-^] and thus ensure the indeterminate root growth. Total 7 samples (2 replicates of shr-2 mutant (high PHABULOSA expression) vs. 2 replicates of shr-2 phb-6 (low/absent PHABULOSA expression). 3 replicates of Wild type used as reference sample.
Project description:Differentiation processes in the primary root meristem are controlled by several signaling pathways that are regulated by phytohormones or by secreted peptides. Long term maintenance of an active root meristem requires that the generation of new root meristem cells and the loss of cells from the meristem due to differentiation is precisely coordinated. Via phenotypic and large scale transcriptome analyses of mutants, we show that the signalling peptide CLE40 and the receptor proteins CLV2 and CRN act in two genetically separable pathways that antagonistically regulate cell differentiation in the proximal root meristem. CLE40 inhibits cell differentiation throughout the primary root meristem by controlling genes with roles in abscisic acid, auxin and cytokinin signalling. CRN and CLV2 jointly control target genes that promote cell differentiation specifically in the transition zone of the proximal root meristem. While CRN and CLV2 are not acting in the CLE40 signaling pathway under normal growth conditions, both proteins are required when the levels of CLE40 or related CLE peptides increase. We show here that two antagonistically acting pathways controlling root meristem differentiation can be activated by the same peptide in a dosage dependent manner.