Transcript profiling of ERF115 transgenic Arabidopsis thaliana
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE48836 | GEO | 2013/11/04
SECONDARY ACCESSION(S): PRJNA212300
REPOSITORIES: GEO
Similar Datasets
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: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: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: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:Plant roots possess a remarkable regenerative potential owing to the presence of stem cells that constantly generate new tissues. Key molecular mechanisms have been linked to this potential, among which the ETHYLENE RESPONSE FACTOR 115 (ERF115) that plays a predominant role in the activation of regenerative cell divisions. However, the downstream operating molecular machinery driving wound-activated cell divisions is largely unknown. Here, we biochemically and genetically identified the GRAS-domain transcription factor protein SCARECROW-LIKE 5 (SCL5) as an interaction partner of ERF115. Although being non-essential under control growth conditions, SCL5 drives redundantly with the related PAT1 and SCL21 transcription factors the expression of the DNA-BINDING ONE FINGER 3.4 (DOF3;4) transcription factor gene. DOF3.4 expression is wound inducible and ERF115 dependent, and in turn activates D3-type cyclin expression. Accordingly, ectopic DOF3.4 expression drives periclinal cell division, whereas its downstream D3-type cyclins are essential for regeneration. The data highlight the importance of the PAT1-branch of GRAS-domain transcription factors for wound activated regeneration processes and pinpoint the DOF3.4 transcription factor as a key element driving regenerative cell divisions.
2023-04-26 | GSE200500 | GEO
Project description:Preceding hypoxia by an ethylene treatment improves root tip survival. To identify key players and processes mediating ethylene enhanced tolerance, the transcriptomic response of root tips was investigated directly after ethylene or control pretreatment, 2 and 4 hours of subsequent hypoxia, and 1 hour of reoxygenation. Seedlings were 4 days or 7 days old and grown on MS plates without added sugar. Only the root tips were harvested
2022-02-01 | E-MTAB-11231 | 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:Flooded plants experience impaired gas diffusion underwater, leading to oxygen deprivation (hypoxia) stress. The volatile plant hormone ethylene is rapidly trapped in submerged plant cells and is instrumental for enhanced metabolic hypoxia acclimation. However, the precise mechanisms underpinning ethylene-enhanced hypoxia survival remain unclear. We studied the effect of ethylene pre-treatment on hypoxia survival of primary Arabidopsis thaliana root tips.
2022-12-19 | PXD031138 | Pride
Project description:Aluminum-dependent stoppage of root growth and terminal differentiation depend on a functional DNA damage response pathway comprised of the master cell cycle checkpoint ATR (ATAXIA TELANGIECTASIA-MUTATED AND RAD3-RELATED) and p53-like transcription factor SOG1 (SUPPRESSOR OF GAMMA RADIATION 1). Mutational loss of either results in failure to trigger endoreduplication following Al treatment even in the Al-hypersensitive mutant, als3-1. Transcriptome analyses were used to identify several Al-induced SOG1-regulated targets as candidate mediators of Al-dependent growth arrest including SMR5, SMR7, ERF114 and ERF115. Analysis of these factors either as loss-of-function/silenced mutants or by overexpression in the als3-1 background indicates ERF115, a key transcription factor involved in stem cell niche restoration, is important for the switch from an actively growing root to one that has terminally differentiated. Consistent with this, a putative ERF115 ortholog and other DDR factors from barley are also upregulated following Al exposure, suggesting a conserved role for this ATR-dependent pathway in response to Al. In contrast to other ts show that ERF115 and related family members are important determinants for the switch to endoreduplication in the root tip following Al exposure and a central output of the ATR-mediated pathway in Al response.
2024-08-27 | GSE222336 | GEO
Project description:APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation
| PRJNA211796 | ENA