Arabidopsis thaliana
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-48836
PROVIDER: PRJNA211796 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells.
2013-11-04 | GSE48793 | GEO
Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells. ChIP-seq analysis of genes bound by the ERF115 transcription factor, using mock ChIP with wild type cells as negative control. Analyzed by Illumina HiSeq
2013-11-04 | E-GEOD-48793 | biostudies-arrayexpress
Project description:This experiment was set up in order to identify the (direct) transcriptional targets of the Ethylene Response Factor 115 (ERF115) transcription factor. Because ERF115 expression occurs in quiescent center (QC) cells and strong effects on the QC cells were observed in ERF115 overexpression plants, root tips were harvested for transcript profiling in order to focus on root meristem and QC specific transcriptional targets.
2013-11-04 | GSE48836 | GEO
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.
2012-12-31 | GSE33015 | GEO
Project description:This experiment was set up in order to identify the (direct) transcriptional targets of the Ethylene Response Factor 115 (ERF115) transcription factor. Because ERF115 expression occurs in quiescent center (QC) cells and strong effects on the QC cells were observed in ERF115 overexpression plants, root tips were harvested for transcript profiling in order to focus on root meristem and QC specific transcriptional targets. Wild-type (Col-0 ecotype), erf115 mutant (SALK_021981) and ERF115 overexpressing (p35S:ERF115 ORF) root tips (three replicates each) were harvested and subjected to transcript profiling, using the Col-0 samples as control reference.
2013-11-04 | E-GEOD-48836 | biostudies-arrayexpress
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.
2012-12-31 | E-GEOD-33015 | biostudies-arrayexpress
Project description:Brassinosteroids (BRs) are steroid hormones involved in multiple processes of plant growth and development, and the adaptation to the environment. Some of the processes regulated by BRs are meristem activity and stem cell divisions. At the core of the root stem cell niche, it is placed the quiescent center (QC), that act as a cell reservoir. QC cells only trigger their divisions when need to replenish the stem cells, for example, after a DNA damage. BR signaling is in charge of triggering these QC divisions, but the exact mechanisms of how this process is regulated is still unknown. Here, we use an interdisciplinary approach, using Arabidopsis thaliana as a model system, including molecular genetics, physiology and bioinformatics to decipher the role of BR receptors upon DNA damage regulating the QC divisions. The results uncover novel roles for the BR-receptor kinase BRL3 (BRI1-like 3) receptor in DNA damage response (DDR) in plants, by modulating the DNA repair and the cell-cycle progression. We identified candidate tissue-specific transcriptional regulator, specifically expressed in the QC cells, the RNR2A (RIBONUCLEOTIDE REDUCTASE 2A), in charge of maintaining dNTPs (deoxynucleotide triphosphates) supply during DNA synthesis that is modulated by BRL3 downstream signaling events. Considering the importance of plant stem cells and their tissues for biomass accumulation and constantly exposed to adverse environmental stresses that can cause DNA damage or cell-cycle arrest in the RAM, here we stablished the mechanism linking root meristematic activity to the DDR through the cell-specific steroid receptor kinase BRL3.
2022-04-02 | GSE199742 | GEO
Project description:Brassinosteroids (BRs) are steroid hormones involved in multiple processes of plant growth and development, and the adaptation to the environment. Some of the processes regulated by BRs are meristem activity and stem cell divisions. At the core of the root stem cell niche, it is placed the quiescent center (QC), that act as a cell reservoir. QC cells only trigger their divisions when need to replenish the stem cells, for example, after a DNA damage. BR signaling is in charge of triggering these QC divisions, but the exact mechanisms of how this process is regulated is still unknown. Here, we use an interdisciplinary approach, using Arabidopsis thaliana as a model system, including molecular genetics, physiology and bioinformatics to decipher the role of BR receptors upon DNA damage regulating the QC divisions. The results uncover novel roles for the BR-receptor kinase BRL3 (BRI1-like 3) receptor in DNA damage response (DDR) in plants, by modulating the DNA repair and the cell-cycle progression. We identified candidate tissue-specific transcriptional regulator, specifically expressed in the QC cells, the RNR2A (RIBONUCLEOTIDE REDUCTASE 2A), in charge of maintaining dNTPs (deoxynucleotide triphosphates) supply during DNA synthesis that is modulated by BRL3 downstream signaling events. Considering the importance of plant stem cells and their tissues for biomass accumulation and constantly exposed to adverse environmental stresses that can cause DNA damage or cell-cycle arrest in the RAM, here we stablished the mechanism linking root meristematic activity to the DDR through the cell-specific steroid receptor kinase BRL3.
2022-04-02 | GSE199741 | GEO
Project description:Entry into and exit from mitosis is driven by precisely-timed changes in protein abundance, and involves transcriptional regulation and protein degradation. However, the role of translational regulation in modulating cellular protein content during mitosis remains poorly understood. Here, using ribosome profiling, we show that translational, rather than transcriptional regulation is the dominant mechanism for modulating protein synthesis at mitotic entry. The vast majority of regulated mRNAs are translationally repressed, which contrasts previous findings of selective mRNA translational activation at mitotic entry. One of the most pronounced translationally repressed genes in mitosis is Emi1, an inhibitor of the anaphase promoting complex (APC), which is degraded during mitosis. We show that Emi1 degradation is insufficient for full APC activation and that simultaneous translational repression is required. These results provide a genome-wide view of protein translation during mitosis and suggest that translational repression may be used to ensure complete protein inactivation Ribosome profiling and mRNA-seq from 3 time points in the cell cycle
2015-09-01 | E-GEOD-67902 | biostudies-arrayexpress
Project description:The anaphase promoting complex/cyclosome (APC/C) is a ubiquitin ligase that controls progression through the eukaryotic cell cycle by targeting key substrates for degradation through the ubiquitin proteasome pathway. During G1, the APC/C works in concert with its co-activator Cdh1 to recognize and ubiquitinate specific substrates during this phase of the cell cycle. While many APC/CCdh1 substrates play a role cell cycle regulation, others are involved in distinct cellular processes, indicating that diverse biological pathways are subject to APC/C-mediated control. To identify novel pathways and substrates regulated by APC/CCdh1, we conducted an unbiased proteomic screen in G1-arrested RPE1 cells acutely treated with small molecule APC/C inhibitors. Combining these results with degron prediction analysis, we discovered a range of putative APC/C substrates. We validated IRS2, a key adaptor protein involved in signaling downstream of the insulin and IGF1 receptors, as a novel direct APC/CCdh1 target. We demonstrate that genetic deletion of IRS2 reduces the expression of proteins involved in cell division and functionally impairs the spindle assembly checkpoint. Together, these findings reveal a novel connection between the insulin/IGF1 signaling network and the cell cycle regulatory machinery.
2020-06-22 | PXD018329 | Pride