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Genome-wide analysis of transcription in dek3 mutants and DEK3-over expressors [8 time points]

ABSTRACT: The decision of whether to grow and proliferate or to restrict growth and develop resilience to stress is a key biological trade-off. Multiple tumour suppressors have roles in suppressing growth and proliferation when conditions are unfavourable, and aggressive tumours show re-wiring of the metabolic pathways and removal of these restraints on growth. In plants, constitutive growth results in increased sensitivity to environmental stress. However, the underlying mechanisms controlling this decision are not well understood. We used temperature as a cue to discover regulators of this process in plants, as it both enhances growth and development rates within a specific range, and is also a stress at extremes. We find the conserved chromatin protein DEK plays a central role in balancing the response between growth and arrest in Arabidopsis, and it does this via H2A.Z-nucleosomes. DEK target genes show two distinct categories of chromatin architecture, and these predict induction or repression by DEK. We show that these chromatin signatures of DEK target genes might be conserved in human cells, suggesting that DEK may act through a fundamental evolutionarily conserved mechanism to control the balance between growth and arrest in plants and animals.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE114641 | GEO | 2024/05/01

REPOSITORIES: GEO

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Genome-wide analysis of transcription in dek3 mutants and DEK3-over expressors [2 temperatures at 2 time points]

Project description:The decision of whether to grow and proliferate or to restrict growth and develop resilience to stress is a key biological trade-off. Multiple tumour suppressors have roles in suppressing growth and proliferation when conditions are unfavourable, and aggressive tumours show re-wiring of the metabolic pathways and removal of these restraints on growth. In plants, constitutive growth results in increased sensitivity to environmental stress. However, the underlying mechanisms controlling this decision are not well understood. We used temperature as a cue to discover regulators of this process in plants, as it both enhances growth and development rates within a specific range, and is also a stress at extremes. We find the conserved chromatin protein DEK plays a central role in balancing the response between growth and arrest in Arabidopsis, and it does this via H2A.Z-nucleosomes. DEK target genes show two distinct categories of chromatin architecture, and these predict induction or repression by DEK. We show that these chromatin signatures of DEK target genes might be conserved in human cells, suggesting that DEK may act through a fundamental evolutionarily conserved mechanism to control the balance between growth and arrest in plants and animals.

2024-05-01 | GSE114418 | GEO

DEK controls the trade-off between growth and arrest via H2A.Z-nucleosomes in Arabidopsis

Project description:The decision of whether to grow and proliferate or to restrict growth and develop resilience to stress is a key biological trade-off. Multiple tumour suppressors have roles in suppressing growth and proliferation when conditions are unfavourable, and aggressive tumours show re-wiring of the metabolic pathways and removal of these restraints on growth1,2. In plants, constitutive growth results in increased sensitivity to environmental stress3,4. However, the underlying mechanisms controlling this decision are not well understood. We used temperature as a cue to discover regulators of this process in plants, as it both enhances growth and development rates within a specific range, and is also a stress at extremes. We find the conserved chromatin protein DEK plays a central role in balancing the response between growth and arrest in Arabidopsis, and it does this via H2A.Z-nucleosomes. DEK target genes show two distinct categories of chromatin architecture, and these predict induction or repression by DEK. We show that these chromatin signatures of DEK target genes might be conserved in human cells, suggesting that DEK may act through a fundamental evolutionarily conserved mechanism to control the balance between growth and arrest in plants and animals.

2024-05-01 | GSE114185 | GEO

GSK3-Mediated Phosphorylation of DEK3 Regulates Chromatin Accessibility and Stress Tolerance in Arabidopsis

Project description:Chromatin dynamics enables the precise control of transcriptional programs. The balance between restricting and opening of regulatory sequences on the DNA needs to be adjusted to prevailing conditions and is fine-tuned by chromatin remodelling proteins. DEK is an evolutionarily conserved chromatin architectural protein regulating important chromatin-related processes. However, the molecular link between DEK-induced chromatin reconfigurations and upstream signalling events remains unknown. Here, we show that ASKβ/AtSK31 is a salt stress-activated Glycogen Synthase Kinase 3 (GSK3) from Arabidopsis thaliana that phosphorylates DEK3. This specific phosphorylation alters nuclear DEK3 protein complex composition, affects nucleosome occupancy and chromatin accessibility that is translated into changes in gene expression, contributing to salt stress tolerance. These findings reveal that DEK3 phosphorylation is critical for chromatin function and cellular stress response and provide a mechanistic example of how GSK3-based signalling is directly linked to chromatin, facilitating a transcriptional response.

2021-09-14 | PXD027308 | Pride

High apoptotic threshold mediates p53 dependent decision between arrest and apoptosis

Project description:In response to stress, the p53 tumor suppressor induces arrest or apoptosis by transcriptionally regulating genes that mediate these processes. It has been proposed that the levels of p53 can influence the choice between these different outcomes, but the mechanisms involved are not clear. To gain mechanistic understanding of this p53-dependent cell fate decision, we generated a p53 inducible system that allowed tight regulation of p53 expression in human mammary epithelial cells. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Using microarray and chromatin immunoprecipitation analysis, we showed that low and high levels of p53 bind to and activate the same set of pro arrest and pro apoptotic target genes, induced to lower and higher levels, respectively. We propose that the cell fate decision between arrest and apoptosis in these cells is determined by a higher threshold required for p53 dependent apoptosis. We suggest that high level p53 activation is crucial in order to achieve maximum efficacy of p53 targeted cancer therapies.

2011-07-19 | E-GEOD-30753 | biostudies-arrayexpress

DEK controls the trade-off between growth and arrest via H2A.Z-nucleosomes in Arabidopsis

Project description:DEK controls the trade-off between growth and arrest via H2A.Z-nucleosomes in Arabidopsis

| PRJNA468415 | ENA

Transcriptional Profiling of Lineage Depleted Dek-KO Murine Bone Marrow Treated with Exogenous DEK

Project description:Nuclear protein DEK is an endogenous DNA-binding chromatin factor regulating hematopoiesis. DEK is one of only two known secreted nuclear chromatin factors, but whether and how extracellular DEK regulates hematopoiesis is not known. We demonstrate that extracellular DEK greatly enhances ex vivo expansion of cytokine-stimulated human and mouse hematopoietic stem cells, and regulates hematopoiesis in vivo and in vitro. These effects are mediated through chemokine receptor CXCR2 and heparan sulfate proteoglycans, and are associated with enhanced phosphorylation of ERK1/2, AKT and p38 MAPK. Thus, DEK acts as a hematopoietic cytokine, with potential for clinical applicability.

2019-02-22 | GSE126875 | GEO

Structural basis of the DEK-nucleosome complex and its functional implications (CUT&Tag)

Project description:The nuclear factor Dek is notably enriched within chromatin; nevertheless, the precise binding mechanism of Dek to the nucleosome remains elusive. In this study, we employ cryo-electron microscopy (cryo-EM) to elucidate the high-resolution structure of the Dek-Nucleosome Core Particle (NCP) complex. We identify specific domains responsible for DEK interaction with the histone octamer and DNA within the nucleosome. The veracity of these binding domains is confirmed through a series of meticulous biochemical experiments. Subsequently, cellular experiments reveal that Dek lacking nucleosome-binding capacity exhibits a deficiency in chromatin interaction. Remarkably, this impairment induces a shift towards the primitive endoderm fate in mouse embryonic stem cells, underscoring the pivotal role of Dek in determining cell fate through its nucleosomal interactions.

2024-01-15 | GSE253062 | GEO

Structural basis of the DEK-nucleosome complex and its functional implications

2023-12-31 | GSE247796 | GEO

Peptide ligand-mediated trade-off between plant growth and stress response

Project description:The decision of whether to grow or to divert energy to stress response is a key physiological trade-off for plants seeking to survive under fluctuating environments. However, the cell-to-cell communication underlying this decision is largely unknown. Here we show that three orphan leucine-rich repeat receptor kinases (LRR-RKs) act as direct ligand-perceiving receptors for PSY-family peptides and play a key role in local switching between two opposing pathways. In contrast to the known LRR-RKs which activate signaling upon ligand binding, PSY receptor (PSYR) signaling, which intrinsically induces a stress response, usually is repressed by ligands to permit growth. Conversely, PSYRs activate the expression of various genes encoding stress response transcription factors upon depletion of the ligands. Loss of PSYRs resulted in defects in the plant’s tolerance to both biotic and abiotic stresses. This ligand-deprivation-dependent activation system enables plants to exert exquisitely tuned regulation of stress responses in the tissues proximal to metabolically dysfunctional damaged sites where ligand production is impaired.

2022-10-14 | GSE208340 | GEO

RNA-Seq of Col-0, dek3-2, dek4-2, and dek3-2 dek4-2 (dd-2) 7-day-old seedlings in Arabidopsis

Project description:Evolutionarily conserved DEK domain-containing proteins have been implicated in multiple chromatin-related processes, mRNA splicing, and transcriptional regulation in eukaryotes. Here, we show that two DEK proteins, DEK3 and DEK4, redundantly control the floral transition in Arabidopsis. DEK3 and DEK4 directly associate with chromatin of related flowering repressors, FLOWERING LOCUS C (FLC), and its two homologs, MADS AFFECTING FLOWERING4 (MAF4) and MAF5, to promote their expression. The binding of DEK3 and DEK4 to histone octamer in vivo affects histone modifications at FLC, MAF4 and MAF5 loci. In addition, DEK3 and DEK4 interact with RNA polymerase II and promote the association of RNA polymerase II with FLC, MAF4 and MAF5 chromatin to promote their expression. Our results show that DEK3 and DEK4 directly interact with chromatin to facilitate the transcription of key flowering repressors and thus prevent precocious flowering in Arabidopsis.

2021-05-04 | GSE163742 | GEO

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