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

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

PROVIDER: PRJNA824837 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18686709_1.fastq.gz	Fastqsanger.gz
	SRR18686709_2.fastq.gz	Fastqsanger.gz
	SRR18686710_1.fastq.gz	Fastqsanger.gz
	SRR18686710_2.fastq.gz	Fastqsanger.gz
	SRR18686711_1.fastq.gz	Fastqsanger.gz

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

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

GaST-seq wounding

Project description:GaST-seq spatial transcriptomics wounding

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Systemic wounding

Project description:Systemic transcriptional responses in Arabidopsis thaliana distal leaves to wounding

2010-04-22 | E-MEXP-2144 | biostudies-arrayexpress

Identification of MKK3-dependent wounding-induced genes

Project description:ra16-01_mkk3_wounding - identification of mkk3-dependent wounding-induced genes - Is MKK3 involved in the transcriptional regulation of wounding-induced genes? - Col and mkk3 KO plants were wounded with a forceps. Leaves were harvested 2h after the stress.

2017-03-10 | GSE95621 | GEO

wt and opr3 control and systemic wounding

Project description:wt plants (ws) and opr3 mutant plants were wounded Half of the rosette leaves of 6 weeks old plants were wounded by clamping a tweezers across the midvein. RNA was extracted from control and systemic leaves 2 h after wounding, and was subject to affymetrix ATH1 chip. one repeat: wt control, wt systemic wounding, opr3 control, opr3 systemic wounding

2010-12-01 | E-GEOD-14332 | biostudies-arrayexpress

Serine protease-mediated wounding identifies localized epidermal wound response genes in Drosophila melanogaster

Project description:We have used trypsin-mediated wounding to amplify the transcriptional response to clean puncture wounding. We studied the transcriptional response of clean puncture wounding and trypsin puncture wounding in relation to unwounded wild-type late-stage embryos. Trypsin puncture wounding generally increases the puncture wounding fold induction relative to unwounded controls.

2013-08-12 | E-MEXP-3755 | biostudies-arrayexpress

AtERF#111/ABR1 is involved in the wounding response

Project description:AtERF#111/ABR1 belongs to the group X of the ERF/AP2 transcription factor family (GXERFs) and is shoot specifically induced under submergence and hypoxia. It was described to be an ABA-response repressor, but our data hint at a completely different function. Here we present evidence that AtERF#111 is involved in the wounding response. Expression profiling of ERF#111-overexpressing (OE) plants demonstrates that AtERF#111 is a transcriptional activator of wounding response genes. Furthermore, direct target genes of AtERF#111 were identified by microarray analyses. However, knockout mutants of AtERF#111 only show a slightly reduced wounding response, suggesting the involvement of other GXERFs in wound signaling and repair mechanisms.

2019-08-28 | GSE121587 | GEO

Transcriptional response to wounding of Arabidopsis thaliana roots

Project description:Time course transcriptional profiling after wounding of 7 day old Arabidopsis roots, cut into 0.3 mm pieces. Samples were taken at 0 h, 1 h, 3 h, 6 h and 12 h after wounding.

2019-11-29 | E-MTAB-7609 | biostudies-arrayexpress

Genome-wilde identification of decapping substrates in the yeast Saccharomyces cervisiae

Project description:To assess the roles of the Dcp2 C-terminal domain and the decapping activators Pat1, Lsm1, and Dhh1 in mRNA decapping, we used RNA-Seq to analyze the expression profiles of yeast cells harboring a truncation of the Dcp2 C-terminal domain, mutations that render Dcp2 catalytically inactive, or deletions of the PAT1, LSM1, and DHH1 genes. Consistent with our recent model for decapping regulation, we found that: i) the Dcp2 C-terminal domain is an effector of both negative and positive regulation and that loss of these control functions causes significant deregulation of mRNA decapping; ii) rather than being global activators of decapping, Pat1, Lsm1, and Dhh1 directly target specific subsets of yeast mRNAs and loss of the functions of each of these factors has substantial indirect consequences for genome-wide mRNA expression; and iii) transcripts targeted by Pat1, Lsm1, and Dhh1 exhibit only partial overlap and, as expected, are targeted to decapping-dependent decay.

2017-12-09 | GSE107841 | GEO

To identify genes that are modulated in keratinocytes in response to wounding.

Project description:Dendritic epidermal T cells (DETC) reside in murine skin and participate in homeostasis and wound repair. Upon wounding, DETC become activated through the recognition of an unidentified ligand expressed by keratinocytes proximal to sites of injury. Such DETC activation is mediated through a monoclonal T cell receptor (TCR). Using a soluble form of this monoclonal TCR, we have shown that keratinocytes upregulate DETC TCR ligands in wounded tissue within 2 hours following wounding. Down-modulation of the ligand is seen 3 hours following wounding, and no expression is evident in non-wounded skin. In vitro studies on cell lines which express this unknown ligand indicate that antigen recognition by the DETC TCR is dependent upon N-linked glycosylation of the ligand. Given the glycosylation sensitivity of the ligand and the restricted expression following wounding, we are interested in pursuing microarray analysis to identify genes that are modulated in keratinocytes in response to wounding.

2011-09-06 | GSE31926 | GEO

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