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Chromatin maps of human ASXL1, FOXK1 and O-GlcNAc

ABSTRACT: Polycomb group (PcG) proteins are major determinants of gene silencing and epigenetic memory in higher eukaryotes. Acting in multimeric protein complexes, these factors control structure and function of chromatin. We used a robust affinity purification mass spectrometry (AP-MS) approach to systematically map the PcG protein interactome in a single human cell line. Importantly, we uncovered the topology map of the human PR-DUB de-ubiquitination complexes, which comprise the O-linked N-acetylglucosamine transferase OGT1 and a number of transcription factors. Here we provide genome-wide chromatin maps of identified PR-DUB1 subunits ASXL1, FOXK1 and the OGT1 catalyzed modification O-GlcNAc based on ChIP-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51673 | GEO | 2016/09/08

SECONDARY ACCESSION(S): PRJNA224307

REPOSITORIES: GEO

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Chromatin maps of human ASXL1, FOXK1 and O-GlcNAc

Project description:Polycomb group (PcG) proteins are major determinants of gene silencing and epigenetic memory in higher eukaryotes. Acting in multimeric protein complexes, these factors control structure and function of chromatin. We used a robust affinity purification mass spectrometry (AP-MS) approach to systematically map the PcG protein interactome in a single human cell line. Importantly, we uncovered the topology map of the human PR-DUB de-ubiquitination complexes, which comprise the O-linked N-acetylglucosamine transferase OGT1 and a number of transcription factors. Here we provide genome-wide chromatin maps of identified PR-DUB1 subunits ASXL1, FOXK1 and the OGT1 catalyzed modification O-GlcNAc based on ChIP-seq. Our data set comprises 3 ChIP-seq samples plus 2 input control samples using chromatin from Flp-In HEK293 T-REx cells cells which was immunoprecipitated using antibodies against ASXL1, FOXK1 and O-GlcNAc.

2016-09-08 | E-GEOD-51673 | biostudies-arrayexpress

Gene regulated by mutant ASXL1 KO and FOXK1/FOXK2 KO in K562 cell line

Project description:Gene regulated by mutant ASXL1 KO and FOXK1/FOXK2 KO in K562 cell line

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Comparative transcriptomic analysis of WT, FOXK1/2 KO, DKO cells and FOXK1 KO cells with reconstitution of several FOXK1 mutants

Project description:The goal of this study was to apply Next Generation Sequencing analyses to identify genes and pathways regulated by the FOXK1 and FOXK2 transcription factor in HeLa cells and to see whether reconstitution of FOXK1 WT and mutants can rescue the altered gene regulation in FOXK1 KO cells. Gene Ontology (GO) analysis did not uncover any dysregulated DNA damage–related pathways upon FOXKs KO. We found that cells reconstituted with any of the three FOXK1 mutants could largely rescue dysregulated gene expression in FOXK1 KO cells, similar to cells reconstituted with WT FOXK1. These suggesting that FOXK1's role in DNA damage response is not by direct transcriptional regulation of DNA damage related pathways and all the three FOXK1 mutants could not affect transcription.

2020-06-26 | GSE151029 | GEO

Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

Project description:Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes via Foxk-Sin3-mediated transcriptional control. Examination of (1) chromatin binding of Foxk1 and Sin3A in non-starved myoblasts and (2) gene expression profiling upon either starvation or siRNA-mediated depletion of Foxk1 relative to a non-starved control.

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RNA-seq datasets from differentiating iHA-Foxk1 and Foxk1 KO mESCs in mesodermal conditions

Project description:D3, D5 and D10 EBs from iHA-Foxk1 and Foxk1 KO cells were harvested for RNA and submitted for sequencing to understand the transcriptional profile of these cells during differentiation in the presence and absence of FOXK1

2023-05-08 | GSE202562 | GEO

ATAC-seq datasets from differentiating iHA-Foxk1 and Foxk1 KO mESCs in mesodermal conditions

Project description:50k cells from D3, D5 and D10 EBs from iHA-Foxk1 and Foxk1 KO cells were harvested for ATAC-seq and submitted for sequencing to understand the chromatin dynamics of these cells during differentiation in the presence and absence of FOXK1

2023-05-08 | GSE202517 | GEO

O-GlcNAcylation of FOXK1 orchestrates the E2F pathway

Project description:Gene transcription is a highly regulated process, and deregulation of transcription factors activity underlie numerous pathologies including cancer. FOXK1 and FOXK2 (FOXK1/2) transcription factors have recently emerged as important regulators of cell metabolism, autophagy and cell differentiation. While FOXK1/2 possesses many overlapping functions in normal biology, their specific functions as well as deregulation of their transcriptional activity in cancer is less clear and often contradictory. FOXK1, but less FOXK2, is known to have oncogenic properties as higher expression levels of FOXK1 has been observed in several cancers and is correlated with tumor progression, invasion, and metastasis. However, the molecular mechanism by which FOXK1 exert its oncogenic properties in caner remains unknown. Here we show that elevated expression of FOXK1, but not FOXK2, in normal human fibroblasts promotes transcription of E2F target genes associated with increased proliferation and delayed senescence entry. Fibroblasts overexpressing FOXK1 are also more prone to cellular transformation with minimal oncogenic combinations, suggesting important oncogenic proprieties of FOXK1. Mechanistically, we found that FOXK1, but not FOXK2, is specifically modified by O-GlcNAcylation. FOXK1 O-GlcNAcylation is modulated during the cell cycle and its highest levels coincides with the G1/S phase transition. Moreover, FOXK1 O-GlcNAcylation is increased following cell transformation and loss of this modification leads to decreased FOXK1 ability to promote cellular transformation and tumor growth. Cells overexpressing FOXK1 O-GlcNAcylation-defective mutants have lower E2F1 expression, cell proliferation, and tumour growth. Our results define a distinct role of FOXK1 via O-GlcNAcylation in controlling the cell cycle through the orchestration of the E2F pathway.

2024-06-10 | PXD050014 | Pride

Tumor-derived neomorphic mutations in ASXL1 impairs the BAP1-ASXL1-FOXK1/K2 transcription network.

Project description:Additional sex combs-like 1 (ASXL1) interacts with BRCA1-associated protein 1 (BAP1) deubiquitinase to oppose the polycomb repressive complex 1 (PRC1)-mediated histone H2A ubiquitylation. Germline BAP1 mutations are found in a spectrum of human malignancies, while ASXL1 mutations recurrently occur in myeloid neoplasm and are associated with poor prognosis. Nearly all ASXL1 mutations are heterozygous frameshift or nonsense mutations in the middle or to a less extent the C-terminal region, resulting in the production of C-terminally truncated mutant ASXL1 proteins. How ASXL1 regulates specific target genes and how the C-terminal truncation of ASXL1 promotes leukemogenesis are unclear. Here, we report that ASXL1 interacts with forkhead transcription factors FOXK1 and FOXK2 to regulate a subset of FOXK1/K2 target genes. We show that the C-terminally truncated mutant ASXL1 proteins are expressed at much higher levels than the wild-type protein in ASXL1 heterozygous leukemia cells, and lose the ability to interact with FOXK1/K2. Specific deletion of the mutant allele eliminates the expression of C-terminally truncated ASXL1 and increases the association of wild-type ASXL1 with BAP1, thereby restoring the expression of BAP1-ASXL1-FOXK1/K2 target genes, particularly those involved in glucose metabolism, oxygen sensing, and JAK-STAT3 signaling pathways. In addition to FOXK1/K2, we also identify other DNA-binding transcription regulators including transcription factors (TFs) which interact with wild-type ASXL1, but not C-terminally truncated mutant. Our results suggest that ASXL1 mutations result in neomorphic alleles that contribute to leukemogenesis at least in part through dominantly inhibiting the wild-type ASXL1 from interacting with BAP1 and thereby impairing the function of ASXL1-BAP1-TF in regulating target genes and leukemia cell growth.

| S-EPMC8225741 | biostudies-literature

Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

2014-11-17 | GSE56932 | GEO

Phase separation mediated transcriptional activity of FOXK1 triggers glycolysis and facilitates renal fibrosis

Project description:Tubular epithelial cells (TECs) undergo an energy metabolism shift from fatty acid oxidation (FAO) to glycolysis in renal fibrosis. The critical pathways leading to the halt of FAO in TECs have been well described, whereas the mechanism underlying the burst of glycolysis remains elusive. We herein reported a critical glycolysis regulator emerged in TECs amid the renal fibrosis, the transcriptional factor forkhead box protein K1 (FOXK1), which exhibited fibrogenic and metabolism-rewiring capacity. Genetic modification of FOXK1 in TECs altered the glycolytic metabolism and fibrotic lesion. The surge of a set of glycolysis-related genes following FOXK1 activation contributed to the energic shift. Nuclear-translocated FOXK1 formed condensates through liquid-liquid phase separation (LLPS) to drive the target genes transcription. The core intrinsically disordered regions (IDRs) within FOXK1 were further mapped and validated. Finally, we explored the therapeutic strategy targeting Foxk1 in the CKD mouse model by subcapsular injecting Foxk1-shRNA-carrying AAV9 vector.

2024-02-29 | GSE253528 | GEO

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