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Genome-wide assay of Vezf1 and RNA Polymerase II binding

ABSTRACT: The protein Vezf1 plays multiple roles important for embryonic development. In Vezf1-/- mouse embryonic stem (MES) cells our earlier data showed widespread changes in gene expression profiles, including decreased expression of the full length active isoform of Dnmt3b methyltransferase and concomitant genome wide reduction in DNA methylation. Here we show that, in HeLaS3 cells, there is a strong genome-wide correlation between Vezf1 binding and peaks of elongating Ser2-P Pol ll, reflecting Vezf1 dependent slowing of elongation. In Wt MES cells the elongating form of RNA polymerase II accumulates near Vezf1 binding sites within the dnmt3b gene and at several other Vezf1 sites, and this accumulation is significantly reduced at these sites in Vezf1-/- MES cells. Depending upon genomic location, Vezf1 mediated Pol II pausing can have different regulatory roles in transcription and splicing. We find examples of genes in which Vezf1 binding sites are located near cassette exons, and in which loss of Vezf1 leads to a change in the relative abundance of alternatively spliced messages. We further show that Vezf1 interacts with Mrg15/Mrgbp, a protein that recognizes H3K36 tri-methylation, consistent with the role of histone modifications at alternatively spliced sites.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE34785 | GEO | 2012/03/09

SECONDARY ACCESSION(S): PRJNA151057

REPOSITORIES: GEO

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Genome-wide assay of Vezf1 and RNA Polymerase II binding

Project description:The protein Vezf1 plays multiple roles important for embryonic development. In Vezf1-/- mouse embryonic stem (MES) cells our earlier data showed widespread changes in gene expression profiles, including decreased expression of the full length active isoform of Dnmt3b methyltransferase and concomitant genome wide reduction in DNA methylation. Here we show that, in HeLaS3 cells, there is a strong genome-wide correlation between Vezf1 binding and peaks of elongating Ser2-P Pol ll, reflecting Vezf1 dependent slowing of elongation. In Wt MES cells the elongating form of RNA polymerase II accumulates near Vezf1 binding sites within the dnmt3b gene and at several other Vezf1 sites, and this accumulation is significantly reduced at these sites in Vezf1-/- MES cells. Depending upon genomic location, Vezf1 mediated Pol II pausing can have different regulatory roles in transcription and splicing. We find examples of genes in which Vezf1 binding sites are located near cassette exons, and in which loss of Vezf1 leads to a change in the relative abundance of alternatively spliced messages. We further show that Vezf1 interacts with Mrg15/Mrgbp, a protein that recognizes H3K36 tri-methylation, consistent with the role of histone modifications at alternatively spliced sites. Comparison of Vezf1 and RNA Pol II binding in mouse and human cells.

2012-03-09 | E-GEOD-34785 | biostudies-arrayexpress

Intragenic DNA methylation prevents cryptic transcription initiations on gene bodies [BS-seq]

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Intragenic DNA methylation prevents cryptic transcription initiations on gene bodies [DECAP-seq]

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Identification of SMCHD1 as a Novel Regulator of Alternative Splicing in FSHD2

Project description:Structural Maintenance of Chromosomes Flexible Hinge Domain Containing 1 (SMCHD1) is a non-canonical member of the structural maintenance of chromosomes (SMC) protein family involved in the regulation of chromatin structure, epigenetic regulation and transcription. Mutations in SMCHD1 cause facioscapulohumeral muscular dystrophy type 2 (FSHD2), a rare genetic disorder characterized by progressive muscle weakness and wasting, believed to be caused by aberrant expression of DUX4 in muscle cells. Here we suggest a new role for SMCHD1 as a regulator of alternative splicing, and demonstrate how splicing alteration caused by SMCHD1 mutations lead to DUX4 expression and FSHD pathogenesis. Analyzing RNA-seq data from muscle biopsies of FSHD2 patients and FSHD2 mouse model found that hundreds of genes were alternatively spliced upon SMCHD1 mutation. At least 20% of alternatively spliced genes were associated with abnormalities of the musculature. Moreover, we show that alternatively spliced exons tend to be bound by SMCHD1, and SMCHD1 bound exons demonstrate slower elongation rate, suggesting SMCHD1 binding promotes exon exclusion by slowing RNAPII. Specifically, we discovered that SMCHD1 mutations promotes the splicing of the DNMT3B1 isoform of DNMT3B, which leads to hypomethylation of the D4Z4 region and DUX4 expression. These results suggest that alternative splicing regulated by SMCHD1 may play a major role in FSHD2 pathogenesis by promoting alternative splicing of different targets including DNMT3B, and highlight the potential for targeting alternative splicing as a therapeutic strategy for this disorder.

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Project description:we performed Native Elongating Transcript Sequencing (NET-seq) on an rpa12Δ strain of S. cerevisiae and evaluated the resultant change in Pol I occupancy throughout the 35S gene and the IGS. Compared to WT, we observed template sequence-specific changes in Pol I occupancy throughout the 35S gene. We also observed rpa12Δ Pol I occupancy downstream of both termination sites and throughout most of the IGS, including the 5S gene. Occupancy of rpa12Δ Pol I increased just upstream of the promoter proximal Reb1 binding site and dropped significantly after, implicating this site as a third terminator for Pol I transcription.

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