Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PAT1-type GRAS-domain proteins control regeneration following wounding by transcriptional activation of DOF3.4 driving cell proliferation

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE200500 | GEO | 2023/04/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Rocks in the Auxin Stream: Wound induced auxin accumulation and ERF115 expression synergistically drive stem cell regeneration

Project description:Plants are known for their outstanding capacity for recovering from various wounds and injury. However, it remains largely unknown how plants sense diverse forms of injury and canalize existing developmental processes into the execution of a correct regenerative response. Auxin, a cardinal plant hormone with morphogenlike properties, has been previously implicated in recovery from diverse types of wounding and organ loss. Here, through a combination of cellular imaging and in silico modelling, we demonstrate that vascular stem cell death obstructs the polar auxin flux, much alike rocks in a stream, and causes it to accumulate in the endodermis. This in turn grants the endodermal cells the capacity to undergo periclinal cell division that repopulate the vascular stem cell pool. Replenishment of the vasculature by the endodermis depends on the transcription factor ERF115, a wound inducible regulator of stem cell divisions. Although not being the primary inducer, auxin is required to maintain ERF115 expression. Reversely, ERF115 sensitizes cells to auxin by activating ARF5/MONOPTEROS, an auxin responsive transcription factor involved in the global auxin response, tissue patterning and organ formation. Combined, the wound induced auxin accumulation and ERF115 expression grant the endodermal cells stem cell activity. Our work provides a mechanistic model for wound induced stem cell regeneration in which ERF115 acts as a wound-inducible stem cell organizer that interprets wound-induced auxin maxima.

2020-06-30 | GSE139715 | GEO

Heat-induced cell damage induces autophagy-mediated cell expansion in Arabidopsis

Project description:Plants have evolved sophisticated cellular and molecular mechanisms to acclimate to adverse environmental stresses. Here, we report that acute heat stress induces excessive cell expansion, reaching up to 13,000 μm2, in Arabidopsis thaliana. The heat-induced cell expansion progressed along with programmed cell death. Autophagy was responsible for excessive cell expansion, as evidenced by autophagic structures in the expanded cells as well as failure of heat-induced cell expansion in autophagy-related 5-1 (atg5-1) and atg7-2 mutants. We also reveal that the transcription factor ETHYLENE RESPONSE FACTOR115 (ERF115), which is activated upon neighboring cell death, is involved in heat-induced cell expansion. ERF115 accumulation in response to heat possibly activated the expression of several ATGs by directly binding to gene promoters. In agreement, the erf115 phytochrome a signal transduction1-2 (pat1-2) double mutant exhibited reduced cell expansion under heat stress with diminished autophagic activity. Overall, our findings indicate that heat-stress-induced cell death triggers autophagy-mediated cell expansion in plant leaves, which may compensate for the death of nearby cells.

2023-11-21 | GSE247997 | GEO

Transcript profiling of ERF115 transgenic Arabidopsis thaliana

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

Transcript profiling of ERF115 transgenic Arabidopsis thaliana

2013-11-04 | GSE48836 | GEO

APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

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

Regulation of transcript abundance and translationny decapping activators Pat1 and Dhh1

Project description:We have examined the roles of yeast mRNA decapping-activators Pat1 and Dhh1 in repressing the translation and abundance of specific mRNAs in nutrient-replete cells using ribosome profiling, RNA-Seq, CAGE analysis of capped mRNAs, RNA Polymerase II ChIP-Seq, and TMT-mass spectrometry of mutants lacking one or both factors. Although the Environmental Stress Response (ESR) is activated in dhh1 and pat1 mutants, hundreds of non-ESR transcripts are elevated in a manner indicating cumulative repression by Pat1 and Dhh1 in WT. These mRNAs show reduced decapping and diminished transcription in the mutants, indicating that impaired mRNA turnover drives transcript derepression in cells lacking Dhh1 or Pat1. mRNA degradation stimulated by Dhh1/Pat1 is not dictated by poor translation nor enrichment for suboptimal codons. Pat1 and Dhh1 also collaborate to reduce translation and protein production from many mRNAs. Transcripts showing concerted translational repression by Pat1/Dhh1 include mRNAs involved in cell adhesion or utilization of the poor nitrogen source allantoin. Pat1/Dhh1 also repress numerous transcripts involved in respiration, catabolism of non-preferred carbon or nitrogen sources, or autophagy; and we obtained evidence for elevated respiration and autophagy in the mutants. Thus, Pat1 and Dhh1 function as post-transcriptional repressors of multiple pathways normally activated only during nutrient limitation.

2023-10-24 | PXD042990 | Pride

Memory of cell divisions directs the continuous process of primitive hematopoietic lineage commitment

Project description:Hematopoietic stem cells (HSCs) exist in a dormant state, and progressively lose regenerative potency as they undergo successive divisions. Why this functional decline occurs and how this information is encoded is unclear. To better understand how this information is stored, we performed RNA sequencing on HSC populations differing only in their divisional history. Comparative analysis revealed that genes upregulated with divisions are enriched for lineage commitment factors, and are regulated by cell cycle-associated transcription factors, indicating that proliferation itself drives primitive hematopoietic lineage priming. In contrast, downregulated genes are associated with an HSC signature and are targeted by the Polycomb Repressive Complex 2 (PRC2). We find that Ezh2 targets HSC signature genes for repression, and a divisional history-dependent switch from Ezh1 to Ezh2 underlies HSC decline with progressive divisions. Thus cell divisions drive lineage priming and Ezh2 accumulation, which represses HSC signature genes and consolidates information on divisional history into memory.

2020-03-14 | GSE145772 | GEO

APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

2013-11-04 | GSE48793 | GEO

Transcription profiling of S. pombe wild type and meu5delta cells during pat1 induced meiosis, wild type meiosis and overexpression of the mei4 transcription factor

Project description:The Meu5 RNA-binding protein stabilises its targets during meiosis. We compared wild type and meu5delta cells transcriptome under different conditions: pat1-induced meiosis in diploid cells, wild type meiosis in diploid cells and cells overexpressing the Mei4 transcription factor.

2011-01-01 | E-TABM-775 | biostudies-arrayexpress

Cell-wall damage activates DOF transcription factors to promote wound healing and tissue regeneration in Arabidopsis thaliana

Project description:Wound healing is a fundamental property of plants and animals that requires recognition of cellular damage to initiate regeneration. In plants, wounding activates a defense response via the production of jasmonic acid and a regeneration response via the hormone auxin and several ethylene response factor (ERF) and NAC domain-containing protein (ANAC) transcription factors. To better understand how plants recognize damage and initiate healing, we searched for factors upregulated during the horticulturally relevant process of plant grafting and found four related DNA binding with one finger (DOF) transcription factors, HIGH CAMBIAL ACTIVITY2 (HCA2), TARGET OF MONOPTEROS6 (TMO6), DOF2.1, and DOF6, whose expression rapidly activated at the Arabidopsis graft junction. Grafting or wounding a quadruple hca2, tmo6, dof2.1, dof6 mutant inhibited vascular and cell-wall-related gene expression. Furthermore, the quadruple dof mutant reduced callus formation, tissue attachment, vascular regeneration, and pectin methylesterification in response to wounding. We also found that activation of DOF gene expression after wounding required auxin, but hormone treatment alone was insufficient for their induction. However, modifying cell walls by enzymatic digestion of cellulose or pectin greatly enhanced TMO6 and HCA2 expression, whereas genetic modifications to the pectin or cellulose matrix using the PECTIN METHYLESTERASE INHIBITOR5 overexpression line or korrigan1 mutant altered TMO6 and HCA2 expression. Changes to the cellulose or pectin matrix were also sufficient to activate the wound-associated ERF115 and ANAC096 transcription factors, suggesting that cell-wall damage represents a common mechanism for wound perception and the promotion of tissue regeneration.

2022-03-23 | GSE179283 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data