Comparison of gene expression in skeletal muscle between Baf155 WT and mutant
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA685843 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13262444_1.fastq.gz | Fastqsanger.gz | |||
| SRR13262444_2.fastq.gz | Fastqsanger.gz | |||
| SRR13262445_1.fastq.gz | Fastqsanger.gz | |||
| SRR13262445_2.fastq.gz | Fastqsanger.gz | |||
| SRR13262446_1.fastq.gz | Fastqsanger.gz |
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Project description:Baf155 is a core subunit of SWI/SNF complex, an ATP dependent chromatin remodeler. To explore the function of Baf155 in skeletal muscle, we deleted the Baf155 in skeletal muscle and compared the gene expression profiling between wild type control and Baf155 deleted mutant mice.
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Project description:CARM1, a coactivator for various cancer-relevant transcription factors, is overexpressed in breast cancer. To elucidate the functions of CARM1 in tumorigenesis, we knocked out CARM1 from several breast cancer cell lines using Zinc-Finger Nuclease technology, which resulted in drastic phenotypic and biochemical changes. The CARM1 KO cell lines enabled identification of novel CARM1 substrates, notably the SWI/SNF core subunit BAF155. Methylation of BAF155 at R1064 was found to be an independent prognostic biomarker for cancer recurrence and to regulate breast cancer cell migration and metastasis. Further, CARM1-mediated BAF155 methylation affects gene expression by directing methylated BAF155 to unique chromatin regions (e.g., c-Myc pathway genes). Collectively our studies uncover a mechanism by which BAF155 acquires tumorigenic functions via arginine methylation. Examination of methylation of BAF155 (R1064) in breast cancer cells
2014-03-28 | E-GEOD-52964 | biostudies-arrayexpress
Project description:During exercise, skeletal muscle is exposed to a low oxygen condition, hypoxia. Under hypoxia, the transcription factor hypoxia-inducible factor-1α (HIF-1α) is stabilized and induces expressions of its target genes regulating glycolytic metabolism. Here, using a skeletal muscle-specific gene ablation mouse model, we show that Brg1/Brm-associated factor 155 (Baf155), a core subunit of the switch/sucrose non-fermentable (SWI/SNF) complex, is essential for HIF-1α signaling in skeletal muscle. Muscle-specific ablation of Baf155 increases oxidative metabolism by reducing HIF-1α function, which accompanies the decreased lactate production during exercise. Furthermore, the augmented oxidation leads to high intramuscular adenosine triphosphate (ATP) level and results in the enhancement of endurance exercise capacity. Mechanistically, our chromatin immunoprecipitation (ChIP) analysis reveals that Baf155 modulates DNA-binding activity of HIF-1α to the promoters of its target genes. In addition, for this regulatory function, Baf155 requires a phospho-signal transducer and activator of transcription 3 (pSTAT3), which forms a coactivator complex with HIF-1α, to activate HIF-1α signaling. Our findings reveal the crucial role of Baf155 in energy metabolism of skeletal muscle and the interaction between Baf155 and hypoxia signaling.
| S-EPMC10396025 | biostudies-literature
Project description:BAF155 ChIP-chip performed on Human Hela S3 Cells for Nimblegen ENCODE arrays which comprise 50mer oligonucleotides spaced every 38bps (overlapping by 12nts). Goal is to identify binding sites for BAF155. Keywords = Transcription Factor Binding, BAF155, ChIP-chip, Human, Genome Tiling Arrays Keywords: ChIP-chip
2005-11-04 | GSE3549 | GEO
Project description:CARM1, a coactivator for various cancer-relevant transcription factors, is overexpressed in breast cancer. To elucidate the functions of CARM1 in tumorigenesis, we knocked out CARM1 from several breast cancer cell lines using Zinc-Finger Nuclease technology, which resulted in drastic phenotypic and biochemical changes. The CARM1 KO cell lines enabled identification of novel CARM1 substrates, notably the SWI/SNF core subunit BAF155. Methylation of BAF155 at R1064 was found to be an independent prognostic biomarker for cancer recurrence and to regulate breast cancer cell migration and metastasis. Further, CARM1-mediated BAF155 methylation affects gene expression by directing methylated BAF155 to unique chromatin regions (e.g., c-Myc pathway genes). Collectively our studies uncover a mechanism by which BAF155 acquires tumorigenic functions via arginine methylation.
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Project description:Comparison Between Sost-CreERT2 and wild type Cre- Gastrocnemius Skeletal Muscle Transcriptomes
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Project description:BAF155, as a component of a chromatin remodeling complex, is thought to be involved in the regulation of gene expression. Baf155 knockdown in ES cells results in misregulation of hundreds of genes (Ho et al., 2009). The Baf155msp3 allele presents a unique case for gene expression analysis wherein the BAF complex appears to be intact, in contrast to disruption of the BAF complex when BAF155 function is lost (Chen and Archer, 2005; Sohn et al., 2007). To examine gene expression in the Baf155msp3 mutant at the time of neural tube closure, we performed RNA-Seq and compared gene expression levels between homozygous wildtype and homozygous mutant embryos. After extensive analysis of the RNA-Seq data comparing all 3 mutants to all 3 WT replicates, 78 genes were identified as being upregulated on average in the mutant samples while 22 genes were downregulated. To facilitate an understanding of global gene expression differences, Ingenuity Pathway Analysis (IPA) was used to assign functional categories to the up- and down-regulated genes in the mutants. The most significant molecular and cellular functions of these genes were: 1. cellular movement (1.46E-04>p>4.12E-02), 2. cell death and survival (2.69E-04>p>4.12E-02), and 3. cell growth and proliferation (2.69E-04>p>3.41E-02). Many neuronal genes were significantly misregulated as well. Overall, the RNA-Seq analysis revealed that surprisingly few genes showed altered expression in Baf155 mutant neural tissue, given the broad epigenetic role of the BAF complex, but included genes involved in neural development and cell survival. Moreover, gene expression changes between individual mutants were variable even though the NTD was consistently observed. This suggests that inconsistent gene regulation contributes to failed neural tube closure. RNA was isolated from somite matched (21-23 somites) and phenotype matched cranial tissue of homozygous wildtype and homozygous mutant embryos (3 of each genotype) at E9.5 just after the time of neural tube closure. At E9.5, the vast majority of the embryonic neural tube is comprised of proliferating neural progenitor cells, constituting a relatively homogeneous cell population.
2014-01-31 | E-GEOD-53459 | biostudies-arrayexpress
Project description:Published study:
https://www.cell.com/cell-reports/fulltext/S2211-1247(20)30789-0
To investigate the influence of lifelong exercise training on human metabolism, we generated global skeletal muscle transcriptomic data from long-term endurance (9 men, 9 women) and strength (7 men) trained individuals. These data were compared with healthy age-matched untrained controls (7 men, 8 women).
| EGAS00001004367 | EGA
Project description:BAF155, as a component of a chromatin remodeling complex, is thought to be involved in the regulation of gene expression. Baf155 knockdown in ES cells results in misregulation of hundreds of genes (Ho et al., 2009). The Baf155msp3 allele presents a unique case for gene expression analysis wherein the BAF complex appears to be intact, in contrast to disruption of the BAF complex when BAF155 function is lost (Chen and Archer, 2005; Sohn et al., 2007). To examine gene expression in the Baf155msp3 mutant at the time of neural tube closure, we performed RNA-Seq and compared gene expression levels between homozygous wildtype and homozygous mutant embryos. After extensive analysis of the RNA-Seq data comparing all 3 mutants to all 3 WT replicates, 78 genes were identified as being upregulated on average in the mutant samples while 22 genes were downregulated. To facilitate an understanding of global gene expression differences, Ingenuity Pathway Analysis (IPA) was used to assign functional categories to the up- and down-regulated genes in the mutants. The most significant molecular and cellular functions of these genes were: 1. cellular movement (1.46E-04>p>4.12E-02), 2. cell death and survival (2.69E-04>p>4.12E-02), and 3. cell growth and proliferation (2.69E-04>p>3.41E-02). Many neuronal genes were significantly misregulated as well. Overall, the RNA-Seq analysis revealed that surprisingly few genes showed altered expression in Baf155 mutant neural tissue, given the broad epigenetic role of the BAF complex, but included genes involved in neural development and cell survival. Moreover, gene expression changes between individual mutants were variable even though the NTD was consistently observed. This suggests that inconsistent gene regulation contributes to failed neural tube closure.
2014-01-31 | GSE53459 | GEO
Project description:Chromatin priming promotes cell type-specific gene expression, lineage differentiation, and development. The mechanism of chromatin priming has not been well understood. Mouse hematopoietic stem and progenitor cells (HSPCs) lacking the Baf155 subunit of the BAF (BRG1/BRM associated factor) chromatin-remodeler produced a significantly reduced number of mature blood cells, leading to a failure of hematopoietic regeneration upon transplantation and 5-FU injury. Baf155 deficient HSPCs, while showing impaired mature blood cell production, generated a higher frequency of myeloid cells with fewer B and CD8+ T cells at homeostasis, supporting a more immune-suppressive tumor microenvironment and enhanced tumor growth. Single-nuclei multi-omic analysis revealed that Baf155 deficient HSPCs failed to establish accessible chromatin and levels of lineage-specific transcripts were considerably lower. Regions that showed a substantial loss in chromatin accessibility were enriched for enhancers and binding motifs for hematopoietic lineage-specific transcription factors. Our study provides a fundamental mechanistic understanding of the role of Baf155 in establishing chromatin priming with functional consequences in regeneration or tumor immunity.
2024-07-09 | GSE240584 | GEO