Sacharomyces cerevisiae Transcript Isoform mapping (set2)
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ABSTRACT:
PROVIDER: PRJNA488283 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Extensive transcriptional heterogeneity revealed by isoform profiling Application of TIF-Seq (Transcript IsoForm Sequencing) to S.cerevisiae. The method was applied to simultaneously identify the 5' capped mRNA transcription start site and the 3' polyadenylation site in different conditions: WT cells grown in glucose media [ypd, 2 biological replicates (bio) and 3 independent library preparations, technical replicates(lib)], WT cells grown in galactose media [ypgal, 4 biological replicates (bio) and 3 independent library preparations, technical replicates(lib)]. A modified protocol designed to enrich in long mRNA molecules was performed for WT cells grown in glucose media [ypd, 2 biological replicates (bio)] and in galactose media [ypgal, 2 biological replicates (bio)] conditions. Finally, control samples performed with a modified protocol designed to identify non-capped but polyadenylated molecules was performed in WT cells grown both in glucose (nypd) and galactose (nypgal) media.
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Project description:Application of TIF-Seq to mutants of the molecular components involved in transcription process.
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Project description:Extensive transcriptional heterogeneity revealed by isoform profiling
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Project description:Saccharomyces cerevisiae Transcript Isoform mapping
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Project description:In cells lacking the histone methyltransferase Set2, initiation of RNA polymerase II transcription occurs inappropriately within the protein-coding regions of genes, rather than being restricted to the proximal promoter. Here, we mapped the transcripts produced in an S. cerevisiae strain lacking Set2, and applied rigorous statistical methods to identify sites of cryptic transcription at high resolution.
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Project description:Application of TIF-Seq to mutants of the molecular components involved in transcription process.
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Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.
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Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.
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Project description:Static gene expression programs have been extensively characterized in stem cells and mature human cells. However, the dynamics of RNA isoform change upon cell-state transitions during cell differentiation, and the determinants and functional consequences have largely remained unclear. Here, we used an improved model for human neurogenesis in vitro that we show is amenable for systems-wide analyses of gene expression. Our multi-omics analysis reveals that the pronounced alterations in cell morphology correlate strongly with widespread changes in RNA isoform expression. Our approach identifies thousands of new RNA isoforms that are expressed at distinct stages during neurogenesis. RNA isoforms mainly arise from the alternative usage of transcription start sites and poly-adenylation sites as well as the skipping of individual exons during human neurogenesis. The transcript isoform changes can remodel the abundance and functions of protein isoforms. Finally, our study identifies a set of RNA-binding proteins as a likely determinant of differentiation stage-specific global isoform changes.
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