Similar Datasets
Project description:Disome-seq data in yeast cells
| PRJNA665694 | ENA
Project description:Genome-wide survey of ribosome collision [monosome/disome]
| PRJNA551384 | ENA
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
Project description:RNA-seq, monosome Ribo-seq, and disome Ribo-seq were performed to study the effect of deletion of ZNF-598 on No-Go mRNA Decay.
2023-11-01 | GSE187348 | GEO
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
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 | GSE98435 | GEO
Project description:Ribosomes that stall before completing peptide synthesis must be recycled and returned to the cytoplasmic pool. The protein Dom34 and cofactors Hbs1 and Rli1 can dissociate stalled ribosomes in vitro, but the identity of targets in the cell is unknown. Here we use ribosome profiling methodology to reveal a high- resolution molecular characterization of Dom34 function in vivo. We show that Dom34 removes stalled ribosomes from mRNAs that are truncated but, in contrast, does not generally dissociate ribosomes on coding sequences known to trigger stalling, such as polyproline. We also show that Dom34 targets arrested ribosomes near the ends of 3 ? UTRs. These ribosomes appear to gain access to the 3 ? UTR via a mechanism that does not require decoding of the mRNA. These results suggest that Dom34 carries out the important task of rescuing ribosomes found in noncoding regions. 25 samples are included in the study (2 mRNA-Seq samples and 23 ribosome footprint profiling samples). These include wild-type and dom34 or hbs1 knockout strains that were created in a variety of genetic backgrounds, treated with various agents in cell culture (e.g. diamide, 3-AT, or glucose starvation), treated differently during cell lysis (use of cycloheximide vs. other ribosome-stabilizing agents), or prepared in different ways after cell lysis (e.g. retention of short vs. long monosome-protected footprints or disome footprints).
2013-12-19 | E-GEOD-52968 | biostudies-arrayexpress
Project description:In protein synthesis, ribosome movement is not always smooth, rather often impeded by numerous reasons. Although the deceleration of ribosome defines the fates of the mRNAs and the synthesizing proteins, fundamental questions remain to be addressed including where ribosomes pause in mRNAs, what kind of RNA/amino acid context causes the pausing, and how physiologically significant the slowdown of protein synthesis is. Here we surveyed the position of ribosome collisions, caused by ribosome pausing, at a genome-wide level using the modified ribosome profiling in human and zebrafish. The collided ribosomes, i.e. disome, emerge at various sites; the proline-proline-lysine motif, stop codons, and 3′ UTR. The number of ribosomes in a collision is not limited to two, rather four to five, forming a queue of ribosomes. Especially, XBP1, a key modulator of unfolded protein response, shows striking queues of collided ribosomes thus acts as a substrate for ribosome-associated quality control (RQC) to avoid the accumulation of undesired proteins in the absence of stress. Our results provide an insight into the causes and the consequences of ribosome slowdowns by dissecting the specific architecture of ribosomes.
2020-05-05 | GSE133393 | GEO
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
Project description:Proteome-wide screening of histone and non-histone Kbz sites in yeast cells
2021-07-19 | PXD027397 | iProX