Regulation of transcriptional interference by the Swi/Snf complex [Mnase-seq]
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ABSTRACT:
PROVIDER: PRJNA956071 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24182104_1.fastq.gz | Fastqsanger.gz | |||
| SRR24182104_2.fastq.gz | Fastqsanger.gz | |||
| SRR24182105_1.fastq.gz | Fastqsanger.gz | |||
| SRR24182105_2.fastq.gz | Fastqsanger.gz | |||
| SRR24182106_1.fastq.gz | Fastqsanger.gz |
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Project description:Alternative transcription start sites regulate transcript isoform diversity and, in turn, often regulate translation levels for a given gene. Recently, a form of gene regulation was described in which transcriptional and translational interference are coordinated, resulting in transcript isoform-dependent changes in protein expression for affected genes. In this form of gene regulation, a long undecoded transcript isoform (LUTI) is transcribed from a gene-distal promoter, interfering with expression of the gene-proximal promoter. While transcriptional and chromatin features associated with LUTI expression have been described, the mechanism underlying LUTI-based transcriptional interference is not well-understood. Using an unbiased genetic approach followed by integrated genomic analysis, we have found that the Swi/Snf chromatin remodeling complex is required for co-transcriptional nucleosome remodeling that leads to LUTI-mediated repression. We uncovered twelve genes with tandem promoters that rely on Swi/Snf function for transcriptional interference during protein folding stress, including three LUTI-regulated genes. Our results provide evidence that, in addition to its canonical function in gene activation, the Swi/Snf complex directly represses promoters that are subject to transcriptional readthrough.
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Project description:RNA-mediated transcriptional silencing prevents deleterious effects of transposon activity and controls the expression of protein-coding genes. It involves long non-coding RNAs (lncRNAs)1, which in Arabidopsis thaliana are produced by a specialized RNA Polymerase V (Pol V)2. lncRNAs guide Argonaute-siRNA complexes to specific genomic loci and mediate the establishment of DNA methylation3,4. The mechanism by which lncRNAs affect chromatin structure and mRNA production remains mostly unknown. Here we identify the SWI/SNF nucleosome remodeling complex as a component of the RNA-mediated transcriptional silencing pathway. We found that SWI3, an essential subunit of the SWI/SNF complex, physically interacts with a lncRNA-binding IDN2 protein5,6. RNA-mediated DNA methylation and transcriptional silencing was compromised in the swi3 mutant. Moreover, targets of SWI/SNF significantly overlapped with genes controlled by Pol V, which shows that the physical interaction reflects a functional relationship. We further found that non-coding transcription by Pol V affects nucleosome positioning on silenced regions. We propose that lncRNAs mediate transcriptional silencing by guiding the SWI/SNF complex and establishing positioned nucleosomes on specific genomic loci. We further propose that guiding ATP-dependent chromatin remodeling complexes may be a more general function of lncRNAs. Mnase-seq of 2 samples (Col-0 and nrpe1).
2012-12-01 | E-GEOD-38401 | biostudies-arrayexpress
Project description:Alternative transcription start sites regulate transcript isoform diversity and, in turn, often regulate translation levels for a given gene. Recently, a form of gene regulation was described in which transcriptional and translational interference are coordinated, resulting in transcript isoform-dependent changes in protein expression for affected genes. In this form of gene regulation, a long undecoded transcript isoform (LUTI) is transcribed from a gene-distal promoter, interfering with expression of the gene-proximal promoter. While transcriptional and chromatin features associated with LUTI expression have been described, the mechanism underlying LUTI-based transcriptional interference is not well-understood. Using an unbiased genetic approach followed by integrated genomic analysis, we have found that the Swi/Snf chromatin remodeling complex is required for co-transcriptional nucleosome remodeling that leads to LUTI-mediated repression. We uncovered twelve genes with tandem promoters that rely on Swi/Snf function for transcriptional interference during protein folding stress, including three LUTI-regulated genes. Our results provide evidence that, in addition to its canonical function in gene activation, the Swi/Snf complex directly represses promoters that are subject to transcriptional readthrough.
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Project description:Alternative transcription start sites regulate transcript isoform diversity and, in turn, often regulate translation levels for a given gene. Recently, a form of gene regulation was described in which transcriptional and translational interference are coordinated, resulting in transcript isoform-dependent changes in protein expression for affected genes. In this form of gene regulation, a long undecoded transcript isoform (LUTI) is transcribed from a gene-distal promoter, interfering with expression of the gene-proximal promoter. While transcriptional and chromatin features associated with LUTI expression have been described, the mechanism underlying LUTI-based transcriptional interference is not well-understood. Using an unbiased genetic approach followed by integrated genomic analysis, we have found that the Swi/Snf chromatin remodeling complex is required for co-transcriptional nucleosome remodeling that leads to LUTI-mediated repression. We uncovered twelve genes with tandem promoters that rely on Swi/Snf function for transcriptional interference during protein folding stress, including three LUTI-regulated genes. Our results provide evidence that, in addition to its canonical function in gene activation, the Swi/Snf complex directly represses promoters that are subject to transcriptional readthrough.
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Project description:Alternative transcription start sites regulate transcript isoform diversity and, in turn, often regulate translation levels for a given gene. Recently, a form of gene regulation was described in which transcriptional and translational interference are coordinated, resulting in transcript isoform-dependent changes in protein expression for affected genes. In this form of gene regulation, a long undecoded transcript isoform (LUTI) is transcribed from a gene-distal promoter, interfering with expression of the gene-proximal promoter. While transcriptional and chromatin features associated with LUTI expression have been described, the mechanism underlying LUTI-based transcriptional interference is not well-understood. Using an unbiased genetic approach followed by integrated genomic analysis, we have found that the Swi/Snf chromatin remodeling complex is required for co-transcriptional nucleosome remodeling that leads to LUTI-mediated repression. We uncovered twelve genes with tandem promoters that rely on Swi/Snf function for transcriptional interference during protein folding stress, including three LUTI-regulated genes. Our results provide evidence that, in addition to its canonical function in gene activation, the Swi/Snf complex directly represses promoters that are subject to transcriptional readthrough.
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Project description:Alternative transcription start sites regulate transcript isoform diversity and, in turn, often regulate translation levels for a given gene. Recently, a form of gene regulation was described in which transcriptional and translational interference are coordinated, resulting in transcript isoform-dependent changes in protein expression for affected genes. In this form of gene regulation, a long undecoded transcript isoform (LUTI) is transcribed from a gene-distal promoter, interfering with expression of the gene-proximal promoter. While transcriptional and chromatin features associated with LUTI expression have been described, the mechanism underlying LUTI-based transcriptional interference is not well-understood. Using an unbiased genetic approach followed by integrated genomic analysis, we have found that the Swi/Snf chromatin remodeling complex is required for co-transcriptional nucleosome remodeling that leads to LUTI-mediated repression. We uncovered twelve genes with tandem promoters that rely on Swi/Snf function for transcriptional interference during protein folding stress, including three LUTI-regulated genes. Our results provide evidence that, in addition to its canonical function in gene activation, the Swi/Snf complex directly represses promoters that are subject to transcriptional readthrough.
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