Integrated Genomic Analysis Reveals Key Features of Long Undecoded Transcript Isoform (LUTI)-based Gene Repression
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ABSTRACT:
PROVIDER: PRJNA588479 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10423736_1.fastq.gz | Fastqsanger.gz | |||
| SRR10423737_1.fastq.gz | Fastqsanger.gz | |||
| SRR10423737_2.fastq.gz | Fastqsanger.gz | |||
| SRR10423738_1.fastq.gz | Fastqsanger.gz | |||
| SRR10423738_2.fastq.gz | Fastqsanger.gz |
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Project description:Long Undecoded Transcript Isoforms (LUTIs) represent a class of non-canonical mRNAs that downregulate gene expression through the combined act of transcriptional and translational repression. While single gene studies revealed some important aspects of LUTI-based repression, how these features impact gene regulation at a global scale is unknown. By using transcript leader and direct RNA sequencing, here we identify 74 LUTI candidates that are expressed specifically during meiotic prophase. Translational repression of these candidates is ubiquitous and dependent on upstream open reading frames. However, LUTI-based transcriptional repression is highly variable. In only 50% of the cases, LUTI transcription causes downregulation of the protein-coding transcript isoform. Higher LUTI expression, enrichment of histone 3 lysine 36 trimethylation, and changes in nucleosome position are the strongest predictors of LUTI-based transcriptional repression. We conclude that LUTIs downregulate gene expression in a manner that integrates translational repression, chromatin state changes, and the magnitude of LUTI expression.
2020-11-01 | GSE140177 | GEO
Project description:Long undecoded transcript isoforms (LUTIs) represent a class of non-canonical mRNAs that downregulate gene expression through the combined act of transcriptional and translational repression. While single gene studies revealed important aspects of LUTI-based repression, how these features affect gene regulation on a global scale is unknown. Using transcript leader and direct RNA sequencing, here, we identify 74 LUTI candidates that are specifically induced in meiotic prophase. Translational repression of these candidates appears to be ubiquitous and is dependent on upstream open reading frames. However, LUTI-based transcriptional repression is variable. In only 50% of the cases, LUTI transcription causes downregulation of the protein-coding transcript isoform. Higher LUTI expression, enrichment of histone 3 lysine 36 trimethylation, and changes in nucleosome position are the strongest predictors of LUTI-based transcriptional repression. We conclude that LUTIs downregulate gene expression in a manner that integrates translational repression, chromatin state changes, and the magnitude of LUTI expression.
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Project description:We used RNA-seq to monitor expression of early meiotic genes and expression of mitotic transcription factor SBF targets. Increased SBF activity was achieved through either overexpression of SBF unique subunit Swi4 , removal of LUTI-mediated regulation of Swi4 levels, or nuclear depeletion of negative regulator of SBF Whi5.
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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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