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BAP1 inhibits the ER stress gene regulatory network and modulates metabolic stress response

ABSTRACT: BRCA1 associated protein 1 (BAP1) is a tumor suppressor with de-ubiquitinating (DUB) enzyme activity and has been implicated in chromatin regulation of gene transcription. The goal of this study is to identify BAP1-dependent transcriptional alterations under both basal (25 mM glucose) and glucose starvation (0 mM glucose) conditions. To this end, we established UMRC6 cell lines (a BAP1 deficient renal cancer cell line) stably expressing Flag-tagged BAP1 wild-type (U6-F), and the empty vector control cells (U6-EV), and performed RNA sequencing (RNA-Seq) analysis in U6-EV and U6-F stable cell lines at 0, 4, and 8 hour upon glucose starvation. The RNA-Seq datasets allow us to compare BAP1-dependent transcriptional alterations under both basal and glucose deprivation conditions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE95097 | GEO | 2017/08/22

SECONDARY ACCESSION(S): PRJNA376054

REPOSITORIES: GEO

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Genome wide binding sites of BAP1, HCF1 and OGT

Project description:We report the genome wide binding sites of BAP1, HCF1 and OGT in bone marrow derived macrophages. De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor–1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans. For BAP1, bone marrow derived macrophages were used differentiated from bone marrow cells of BAP1-3X Flag Tagged KI mice we generated. For OGT and HCF1, bone marrow derived macrophages were used from BAP1 WT mice.

2012-11-07 | E-GEOD-40723 | biostudies-arrayexpress

Specific biomarkers for stochastic division patterns and starvation-induced quiescence under limited glucose levels in fission yeast

Project description:Glucose as a source of energy is centrally important to our understanding of life. We investigated the cell division-quiescence behavior of the fission yeast Schizosaccharomyces pombe under a wide range of glucose concentrations (0-111 mM). The mode of S. pombe cell division under a microfluidic perfusion system was surprisingly normal under highly diluted glucose concentrations (5.6 mM, 1/20 of the standard medium, within human blood sugar levels). Division became stochastic, accompanied by a curious division-timing inheritance, in 2.2-4.4 mM glucose. A critical transition from division to quiescence occurred within a narrow range of concentrations (2.2-1.7 mM). Under starvation (1.1 mM) conditions, cells were mostly quiescent and only a small population of cells divided. Under fasting (0 mM) conditions, division was immediately arrested with a short chronological lifespan (16 h). When cells were first glucose starved prior to fasting, they possessed a substantially extended lifespan (∼14 days). We employed a quantitative metabolomic approach for S. pombe cell extracts, and identified specific metabolites (e.g. biotin, trehalose, ergothioneine, S-adenosyl methionine and CDP-choline), which increased or decreased at different glucose concentrations, whereas nucleotide triphosphates, such as ATP, maintained high concentrations even under starvation. Under starvation, the level of S-adenosyl methionine increased sharply, accompanied by an increase in methylated amino acids and nucleotides. Under fasting, cells rapidly lost antioxidant and energy compounds, such as glutathione and ATP, but, in fasting cells after starvation, these and other metabolites ensuring longevity remained abundant. Glucose-starved cells became resistant to 40 mM H(2)O(2) as a result of the accumulation of antioxidant compounds.

2017-07-06 | MTBLS316 | MetaboLights

Genome wide binding sites of BAP1, HCF1 and OGT

2012-11-07 | GSE40723 | GEO

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Project description:Proteome data obtained with timsTOF Pro of the fission yeast cells exposed to glucose starvation at four time points 0 (glucose rich conditions), 15, 60 and 120 minutes

2023-07-01 | MSV000092327 | MassIVE

BAP1 links epigenetic regulation of ferroptosis to tumor suppression

Project description:Compared to the well-established roles of apoptosis in tumor suppression, the roles and regulatory mechanisms of ferroptosis, a non-apoptotic form of cell death, in tumor biology remain much less understood. BRCA1-associated protein 1 (BAP1) encodes a nuclear de-ubiquitinating (DUB) enzyme to reduce histone 2A ubiquitination (H2Aub) on chromatin, and is a tumor suppressor in several human cancers. Here, integrated transcriptomic, epigenomic, and cancer genomic analyses link BAP1 to metabolism-related biological processes, including oxidative stress response, and identify cystine transporter SLC7A11 as a BAP1-repressed target gene with high relevance to BAP1-mediated tumor suppression in human cancers. Functional studies reveal that BAP1, in a DUB-dependent manner, decreases H2Aub occupancy on the SLC7A11 promoter and represses SLC7A11 expression, and that BAP1 inhibits cystine uptake and promotes ferroptosis through repressing SLC7A11 expression. Finally, we show that BAP1 inhibits tumor development partly through SLC7A11, and that cancer-associated BAP1 mutants lose their abilities to repress SLC7A11 and to promote ferroptosis. Together, the results of our study show that BAP1 executes its tumor suppression function at least partly through its regulation of SLC7A11 and ferroptosis, and uncover a previously unappreciated mechanism coupling ferroptosis to tumor suppression.

2018-07-05 | GSE101987 | GEO

RNA-Seq of the murine hypothalamic cell line mHypoA-2/10 after glucose stimulation

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2021-07-05 | E-MTAB-10629 | biostudies-arrayexpress

long non-coding RNA GDAR regulate ovine granulosa cells apoptosis by affecting the expression of apoptosis-related genes

Project description:Short-term dietary supplementation of female sheep during the luteal phase can increase fertility and most probably by stimulating glucose uptake by the follicles. However, the molecular mechanism of glucose regulates follicular development has not yet been clarified, especially the further study of long non-coding RNA (lncRNA) in determining fertility during follicular development. We generated GCs models of different doses of glucose (0, 2.1, 4.2, 8.4, 16.8 and 33.6 mM), and observed that the highest cell viability was recorded in the 8.4 mM group and the highest apoptosis rates were recorded in the 33.6 mM groups. Therefore, the control (n = 3, 0 mM glucose group), low glucose (n = 3, add 8.4 mM glucose concentration group), and high glucose (n = 3, add 33.6 mM glucose concentration group) of GCs were created for the next whole genomic RNA sequencing (RNA-seq). In total, 11,221 novel lncRNAs and 510 annotated lncRNAs were identified in the GCs samples. Gene ontology term enrichment indicates the obvious enrichment in apoptosis and its related pathways, which suggests that cell apoptosis could play a critical role in the process of glucose-induced GCs differentiation. Furthermore, we focused on the function of a lncGDAR and verified that lncGDAR could involve cell apoptosis by effecting the expression of Bcl-2, BAX, Caspase-3, and Caspase-7 genes. These results provide the basis for further study of LncRNA regulation mechanism in nutrition on female fertility.

2022-05-18 | GSE200668 | GEO

Inactivation of Bap1 Cooperates with Losses of Nf2 and Cdkn2a to Drive the Development of Pleural Malignant Mesothelioma in Conditional Mouse Models

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2019-05-30 | GSE131942 | GEO

Stress responses elicited by glucose withdrawal in Aspergillus fumigatus

Project description:Glucose is a widely used carbon source in laboratory practice to culture Aspergillus fumigatus, however, glucose availability is often low in its “natural habitats” including the human body. We used a physiological–transcriptomical approach to reveal differences between A. fumigatus Af293 cultures incubated on glucose, glucose and peptone, peptone (carbon limitation), or without any carbon source (carbon starvation). Autolytic cell wall degradation was upregulated by both carbon starvation and limitation. The importance of autolytic cell wall degradation in adaptation to carbon stress was also highlighted by approximately 12.4% of the A. fumigatus genomes harbor duplication of genes involved in N-acetyl glucosamine utilization. Glucose withdrawal increased redox imbalance, altered both the transcription of antioxidative enzyme genes and oxidative stress tolerance, downregulated iron acquisition, but upregulated heme protein genes. Transcriptional activity of the Gliotoxin cluster was low in all experiments, while the Fumagillin cluster showed substantial activity both on glucose and under carbon starvation, and the Hexadehydro-astechrome cluster only on glucose. We concluded that glucose withdrawal substantially modified the physiology of A. fumigatus including processes that contribute to virulence. This may explain the challenge of predicting the in vivo behavior of A. fumigatus based on data from glucose rich cultures.

2022-12-09 | GSE216000 | GEO

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Project description:Transcriptional profiling of Enterococcus faecalis V583 comparing the transcriptome of cells grown in M17 + glucose 0.5% (GM17) with the transcriptome of cells grown in M17 + glucose 0.5% + 0.05 mM CuSO4

2011-08-22 | GSE30949 | GEO

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