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RNA Seq analysis of WT haploid and Disome 10 in Saccharomyces cerevisiae

ABSTRACT: Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE98435 | GEO | 2017/09/12

SECONDARY ACCESSION(S): PRJNA385090

REPOSITORIES: GEO

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ChIP Seq analysis of H3K4me3 and H3K79me3 in euploid and aneuploid Saccharomyces cerevisiae

Project description:Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.

2017-09-12 | GSE98282 | GEO

Disome-seq data in yeast cells

Project description:Genome-wide detection of monosome and disome distributions in yeast cells

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Disome-seq data in yeast cells

Project description:Disome-seq data in yeast cells

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Disome and trisome profiling reveal targets of ribosome quality control

Project description:The ribosome-associated protein quality control (RQC) system that resolves stalled translation events is activated when ribosomes collide and form disome, trisome or higher order complexes. However, it is unclear whether this system distinguishes collision complexes formed on defective mRNAs from those with functional roles on endogenous transcripts. Here, we performed disome and trisome footprint profiling in yeast and found collisions were enriched on diverse sequence motifs known to slow translation. When 60S recycling was inhibited, disomes accumulated at stop codons and could move into the 3’UTR to reinitiate translation. The ubiquitin ligase and RQC factor Hel2/ZNF598 generally recognized collisions but did not trigger degradation of endogenous transcripts. However, loss of Hel2 triggered the integrated stress response, via phosphorylation of eIF2alpha, thus linking these pathways. Our results suggest that Hel2 has a role in sensing ribosome collisions on endogenous mRNAs and such events may be important for cellular homeostasis.

2020-05-26 | GSE139036 | GEO

Monosome and disome profiling of Flag-STAU1 Flp-In 293 T-REx cells

Project description:Monosome and disome profiling was performed on Flag-STAU1 Flp-In 293 T-REx to study the causes of ribosomal collisions, and whether this may be modulated by the presence/absence of Staufen-1. Cells were treated with either an siRNA targeting STAU1 transcript (4x samples) or a control siRNA (2x samples). Two of the four samples treated with the STAU1 siRNA had siRNA-resistant STAU1 mRNA expression induced by doxycycline (rescue). Sequencing libraries from monosome and disome fractions were generated in parallel from the same samples. Note that unique molecular identifiers/random barcodes (UMIs/RBCs) were included in the sequencing experiment. Each UMI has been moved to the fastq read name of each read. For example \\"xxxxxxrbc:AGCCAAT\\" in the read name signifies that the given read had a UMI of \\"AGCCAAT\\". Using these UMIs, PCR duplicates can be removed with UMI-Tools following read alignment.

2023-04-30 | E-MTAB-9669 | biostudies-arrayexpress

Genome-wide survey of ribosome collision [monosome/disome]

Project description:Genome-wide survey of ribosome collision [monosome/disome]

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Chromatin rewiring mediates programmed evolvability via aneuploidy

Project description:Eukaryotes have evolved elaborate mechanisms to ensure that chromosomes segregate with high fidelity during mitosis and meiosis, and yet specific aneuploidies can be adaptive during environmental stress. Here, we identify a chromatin-based system for inducible aneuploidy in a human pathogen. Candida albicans utilizes chromosome missegregation to acquire resistance to antifungal drugs and for ploidy reduction after mating. We discovered that the ancestor of C. albicans and two related pathogens evolved a variant of histone H2A that lacks the conserved phosphorylation site for Bub1 kinase, a key regulator of chromosome segregation. Using engineered strains, we show that expression of this variant controls the rates of aneuploidy and antibiotic resistance in this species. Moreover, whole genome chromatin precipitation analysis reveals that CENP-A/Cse4, the histone H3 that specifies centromeres, is depleted from tetraploid mating products and virtually eliminated from cells exposed to aneuploidy-promoting cues. Thus, changes in chromatin regulation can confer the capacity for rapid evolution in eukaryotes.

2019-05-23 | GSE122037 | GEO

Disome-seq reveals sequence-mediated coupling of translational pauses and protein structures

Project description:The regulation of translation elongation plays a vital role in protein folding; an adequate translational pause provides time and cellular environments for the co-translational folding of nascent peptides. However, the genomic landscape, sequence determinants, and molecular consequences of translational pausing remain mostly unknown. In this study, we performed disome-seq that sequenced mRNA fragments protected by two consecutive ribosomes – a product of severe translational pauses during which the upstream ribosome collides into the paused one. We detected severe translational pauses on ~75% of yeast genes. These pauses were often explained by one of the three mechanisms: 1) slow ribosome releasing at stop codons, 2) slow peptide formation from proline, glycine, asparagine, and cysteine, and 3) slow leaving of polylysine from the exit tunnel of ribosomes. Notably, these amino acids also terminate the α-helical conformation. Such dual roles of amino acids establish an inborn coupling between the synthetic completion of a structural motif and a translational pause. Furthermore, paused ribosomes often recruit chaperones to assist protein folding. As a consequence, emergent protein structures during evolution should be ready to be correctly folded. Collectively, our study shows widespread translational pauses and sheds lights on a better understanding of the regulation of co-translational protein folding.

2020-12-10 | PXD015271 | Pride

A NOVEL EPIGENETIC SILENCING PATHWAY INVOLVING the HIGHLY CONSERVED 5'-3' EXORIBONUCLEASE Dhp1/Rat1/Xrn2 in SCHIZOSACCHAROMYCES POMBE [CRAC-seq]

Project description:Epigenetic gene silencing plays a critical role in regulating gene expression and contributes to organismal development and cell fate acquisition in eukaryotes. In fission yeast, Schizosaccharomyces pombe, heterochromatin-associated gene silencing is known to be mediated by RNA processing pathways including RNA interference (RNAi) and a 3’-5’ exoribonuclease complex exosome. Here, we report a new RNA-processing pathway that contributes to epigenetic gene silencing and assembly of heterochromatin mediated by 5’-3’ exoribonuclease Dhp1/Xrn2. Dhp1 mutation causes defective gene silencing both at peri-centromeric regions and at the silent mating type locus. Intriguingly, mutation of either one of two well-characterized Dhp1-interacting proteins, the Din1 pyrophosphohydrolase or the Rhn1 transcription termination factor, does not show silencing defects at the main heterochromatic regions. Dhp1 is essential in the sequential steps of establishing silencing in a manner independent of both RNAi and the exosome. Genomic and genetic analysis suggest that Dhp1 is involved in post-transcriptional silencing of repetitive regions through its catalytic activity. Our study is the first investigation into an unexpected role of Dhp1/Rat1/Xrn2 in chromatin-based silencing. These results elucidate how various RNA-processing pathways, acting together or independently, contribute to epigenetic regulation of the eukaryotic genome.

2016-01-28 | GSE77290 | GEO

A NOVEL EPIGENETIC SILENCING PATHWAY INVOLVING the HIGHLY CONSERVED 5'-3' EXORIBONUCLEASE Dhp1/Rat1/Xrn2 in SCHIZOSACCHAROMYCES POMBE [gene expression]

2016-01-28 | GSE77289 | GEO

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