Comparison of gene expression in skeletal muscle between Baf155 WT and mutant
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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: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
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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.
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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.
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Project description:Post-translational modifications (PTMs) of chromatin remodelers are abundant but functionally understudied. Here we investigate the role of asymmetric dimethylation of arginine 1064 (BAF155me2a) on the SWI/SNF core subunit BAF155, a mark deposited by CARM1/PRMT4 that has been linked to tumor progression but whose molecular function remains unclear. Using immunoprecipitation–mass spectrometry with a dimethyl-specific antibody, we found that R1064me2 selectively enhances BAF155 interactions with RNA processing factors, including the anti-termination protein SCAF4, splicing factors, and the transcription factor RFX5. CUT&RUN profiling showed that BAF155me2a, SCAF4, and RFX5 co-occupy promoter regions, and reciprocal immunoprecipitations confirmed that the SCAF4–BAF155 interaction depends on R1064 methylation. To test the functional consequences of this modification, we generated cells expressing either wild-type BAF155 or a methylation-deficient BAF155-R1064K mutant. Loss of methylation did not alter chromatin accessibility, BAF155 genomic occupancy, or SCAF4 recruitment. However, nascent transcription measured by TT-seq revealed a coordinated reduction in 5′ sense transcripts and upstream antisense transcripts (PROMPTs) at BAF155-bound promoters, with a quantitatively larger decrease in PROMPTs at SCAF4 co-bound sites. The effect was restricted to the promoter-proximal region and resolved toward the gene end, consistent with a defect in productive elongation downstream of RNA polymerase II recruitment. These data support a model in which BAF155 dimethylation provides a co-transcriptional interface coupling SWI/SNF to RNA processing machinery, and identify regulation of nascent transcription as a non-canonical function of SWI/SNF PTMs.
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Project description:Post-translational modifications (PTMs) of chromatin remodelers are abundant but functionally understudied. Here we investigate the role of asymmetric dimethylation of arginine 1064 (BAF155me2a) on the SWI/SNF core subunit BAF155, a mark deposited by CARM1/PRMT4 that has been linked to tumor progression but whose molecular function remains unclear. Using immunoprecipitation–mass spectrometry with a dimethyl-specific antibody, we found that R1064me2 selectively enhances BAF155 interactions with RNA processing factors, including the anti-termination protein SCAF4, splicing factors, and the transcription factor RFX5. CUT&RUN profiling showed that BAF155me2a, SCAF4, and RFX5 co-occupy promoter regions, and reciprocal immunoprecipitations confirmed that the SCAF4–BAF155 interaction depends on R1064 methylation. To test the functional consequences of this modification, we generated cells expressing either wild-type BAF155 or a methylation-deficient BAF155-R1064K mutant. Loss of methylation did not alter chromatin accessibility, BAF155 genomic occupancy, or SCAF4 recruitment. However, nascent transcription measured by TT-seq revealed a coordinated reduction in 5′ sense transcripts and upstream antisense transcripts (PROMPTs) at BAF155-bound promoters, with a quantitatively larger decrease in PROMPTs at SCAF4 co-bound sites. The effect was restricted to the promoter-proximal region and resolved toward the gene end, consistent with a defect in productive elongation downstream of RNA polymerase II recruitment. These data support a model in which BAF155 dimethylation provides a co-transcriptional interface coupling SWI/SNF to RNA processing machinery, and identify regulation of nascent transcription as a non-canonical function of SWI/SNF PTMs.
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