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Tuning of the RBR1-E2F/DP transcriptional module bythe F- box protein FBL17

ABSTRACT: F-box proteins of SCF E3 ligases have been documented to control the abundance of numerous critical regulatoryproteins. In Arabidopsis, one of them, F-BOX- LIKE17 (FBL17), stands out for playing a key role in DNA replication,DNA damage, and, more recently, for the control of cell size. FBL17 null mutants exhibit severe cellular defectsleading to lethality. However, the molecular mechanisms by which FBL17 operate remain poorly understood.Here, we show that FBL17 interacts with different components of the RETINOBLASTOMA-RELATED1/E2F moduleand is involved in the protein turnover of E2Fa and E2Fb. However, mutations in E2Fa or E2Fb do not alleviate thesevere fbl17 phenotype but worsen it. By contrast, it is the accumulation of the transcriptional repressor E2Fc thatcauses fbl17 mutant lethality. Our results highlight a key role for FBL17 in modulating the transcriptional controlof E2F target genes ensuring precise control of cell cycle progression and avoiding uncontrolled DNA damage re-sponse.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE328429 | GEO | 2026/04/18

REPOSITORIES: GEO

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RBR1-E2F/DP transcriptional regulation modulated by the F-box protein FBL17

Project description:In all eukaryotes, F-box proteins of SCF E3 ligase complexes have been well-documented to control the abundance of numerous critical regulatory proteins. In Arabidopsis, one of them, F-BOX-LIKE17 (FBL17), stands out for playing a key role in DNA replication, DNA damage and more recently for the control of cell size. FBL17 null mutants exhibit severe cellular defects leading to lethality, presumably due to impaired degradation of cyclin-dependent kinase inhibitor proteins. However, the molecular mechanisms by how FBL17 operate remain poorly understood. Here we show that FBL17 interacts with different components of the RETINOBLASTOMA-RELATED1/E2F module. In particular, FBL17 directly targets the two transcription factors E2Fa and E2Fb and is involved in their protein turnover. However, it is the transcriptional repressor E2Fc, which is not a substrate of FBL17, that causes fbl17 mutant lethality. Hence, the e2fc mutation broadly suppresses cell elongation and cell proliferation defects observed in fbl17. Moreover, in the fbl17 e2fb double mutant the strong overexpression of DNA damage genes is significantly attenuated through RBR1 recruitment to its target genes. Altogether, our results highlight a key role for FBL17 in modulating the transcriptional control of E2F-target genes ensuring precise control of cell cycle progression and avoiding uncontrolled DNA damage response.

2026-02-23 | PXD063507 | Pride

Arabidopsis E2F target genes

Project description:Entry into the S phase of the cell cycle is controlled by the E2F transcitption factors that induce the transcription of genes required for cell cycle progression and DNA replication. To identify E2F target genes of Arabidopsis on a genome-wide scale, the transcriptome of wild-type plants was compared with that one of plants ectopically expressing the E2Fa-DPa genes. In four independent experiments, E2Fa-DPa overexpressing plants were grown side-to-side with wild type (Col-0) plants. RNA was extracted from 6-day-old seedlings. Each biological sample was harvested and processed independently, and finally all probed individually to Affymetrix ATH1 microarrays, resulting into 8 hybridization signals for each probeset. Experimenter name = Lieven De Veylder; Experimenter phone = +32 9 3313961; Experimenter fax = +32 9 3313809; Experimenter address = Technologiepark 927; Experimenter address = B-9052 Gent; Experimenter zip/postal_code = B-9052; Experimenter country = Belgium Experiment Overall Design: 8 samples were used in this experiment

2008-06-13 | E-GEOD-5529 | biostudies-arrayexpress

Arabidopsis E2F target genes

Project description:Entry into the S phase of the cell cycle is controlled by the E2F transcitption factors that induce the transcription of genes required for cell cycle progression and DNA replication. To identify E2F target genes of Arabidopsis on a genome-wide scale, the transcriptome of wild-type plants was compared with that one of plants ectopically expressing the E2Fa-DPa genes. In four independent experiments, E2Fa-DPa overexpressing plants were grown side-to-side with wild type (Col-0) plants. RNA was extracted from 6-day-old seedlings. Each biological sample was harvested and processed independently, and finally all probed individually to Affymetrix ATH1 microarrays, resulting into 8 hybridization signals for each probeset. Experimenter name = Lieven De Veylder Experimenter phone = +32 9 3313961 Experimenter fax = +32 9 3313809 Experimenter address = Technologiepark 927 Experimenter address = B-9052 Gent Experimenter zip/postal_code = B-9052 Experimenter country = Belgium Keywords: genetic_modification_design

2006-08-15 | GSE5529 | GEO

Tuning of the RBR1-E2F/DP transcriptional module bythe F- box protein FBL17

Project description:Tuning of the RBR1-E2F/DP transcriptional module bythe F- box protein FBL17

| PRJNA1454953 | ENA

Benchmark study of different chromatin isolation methods using the E2Fa transcription factor

Project description:Genome-wide identification of transcription factor (TF) binding sites is pivotal to our understanding of gene expression regulation. Although much progress has been made in the determination of potential binding regions of proteins by chromatin immunoprecipitation (ChIP), this method has some inherent limitations regarding DNA enrichment efficiency and antibody necessity. Here, we report an alternative strategy for assaying in vivo TF-DNA binding in Arabidopsis thaliana cells by tandem chromatin affinity purification (TChAP). Evaluation of TChAP using the E2Fa TF and comparison with traditional ChIP and single chromatin affinity purification illustrates the suitability of TChAP and provides a resource for exploring the E2Fa transcriptional network. Integration with transcriptome, cis-regulatory element, functional enrichment, and co-expression network analyses demonstrates the quality of the E2Fa TChAP-seq data and validates the identification of new direct E2Fa targets. TChAP enhances both TF target mapping throughput, by circumventing issues related to antibody availability, and output, by improving DNA enrichment efficiency.

2014-02-04 | GSE53422 | GEO

Benchmark study of different chromatin isolation methods using the E2Fa transcription factor

2014-02-04 | E-GEOD-53422 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:Transcriptome analysis of Arabidopsis plants lacking all three E2F isoforms, E2FA, E2FB, and E2FC

| PRJDB14792 | ENA

E2F regulation of Phosphoglycerate kinase (Pgk) gene is functionally important in Drosophila development

Project description:Our study focuses on understanding the changes in chromatin accessibility in the Pgk-DeltaE2F mutant that takes place during flight muscles development in Drosophila. E2F binding sites were mutated upstream Pgk gene. E2F/Dp/Rbf were no longer recruited to this regulatory region. As a result of this, the expression of Pgk mRNA was downregulated, which led to reduced levels in many metabolites that are glycolytic and TCA intermediates. Using ATAC-seq we determined that there was a global reduction in chromatin accessibility in the mutant compared to control, and it was accompagnied by a widespread reduction in gene expression, including metabolic genes. In addition we identified a broad range of phenotypes when analyzing the functional relevance of E2F regulation on Pgk gene. These phenotypes range from low ATP content, abnormal mitochondrial morphology, shortened life span to embrionic lethality. Furthermore, defects in high-energy consuming organs, such as ovaries and muscles, were found. In sum, our results illustrate the pleiotropic effects on metabolism, gene expression and development in the Pgk-deltaE2F animals, which underlies the importance of E2F regulation on a single E2F target, Pgk.

2023-03-20 | GSE217225 | GEO

SILAC-iPOND analysis of WT vs ATRX KO eHAP cells ± HU

Project description:Mutations in the ATRX chromatin remodeller predispose to a developmental genetic disorder and cancer, but how ATRX safeguards genome and telomere stability remains unresolved. Here, we uncover critical dependencies for the CTC1-STN1-TEN1 (CST) complex and RAD9A-HUS1-RAD1 (9-1-1) clamp in ATRX deficient cells. ATRX:CST synthetic lethality manifests following accumulation of telomeric G-rich ssDNA, which results in telomere loss and cell death. Conversely, we attribute ATRX:9-1-1 synthetic lethality to genome-wide ssDNA lesions, which compromise DNA replication. We further show that ATRX suppresses DNA damage during replication stress by counteracting the activity of the FAM111A protease. We demonstrate that roles of ATRX in telomere maintenance and replication are genetically separable, requiring its ATPase activity and PIP-box, respectively. We also show that such roles protecting genome stability are largely independent of the ATRX-DAXX interaction. Collectively, our data show that functions of ATRX in suppressing toxic ssDNA lesions are context-dependent and are key to global DNA replication and telomere integrity.

2026-05-19 | PXD068487 | Pride

The impact of E2F/Dp inactivation on metabolism differs between muscles and fat body cells

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2021-02-11 | MSV000086854 | MassIVE

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