Ribosome profiling and RNA sequencing of MCF10A cells treated with torin or by serum starvation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59816 | GEO | 2016/02/17
SECONDARY ACCESSION(S): PRJNA256320
REPOSITORIES: GEO
Similar Datasets
Project description:MCF10A were either untreated, treated with torin or by starvation, to induce autophagy. RNA sequencing and ribosome profiling was performed. 1 biological replicate for each condition
2016-02-17 | E-GEOD-59816 | biostudies-arrayexpress
Project description:MCF10A were either untreated or treated with TGFb. RNA sequencing and ribosome profiling was performed.
2017-07-27 | GSE59817 | GEO
Project description:To knock down SLC3A2, MCF10A cells were either transfected with control siRNAs, or siRNAs specifically targetting SLC3A2. Samples were either untreated or treated with TGFb. Ribosome profiling and RNA sequencing was performed on these samples. MCF10A cells with and without SLC3A2 overexpression construct were either untreated or treated with TGFb. Ribosome profiling was performed on these samples.
2017-07-27 | GSE59818 | GEO
Project description:We have performed parallel ribosome profiling and RNA sequencing to determine which mRNAs are being translated during exponential growth and following 24 hours of nutrient starvation in the human pathogen Mycobacterium tuberculosis.
2021-02-02 | E-MTAB-8835 | biostudies-arrayexpress
Project description:Ribosome profiling and RNA sequencing of MCF10A cells treated with torin or by serum starvation
| PRJNA256320 | ENA
Project description:Ribosome profiling of Mycobacterium tuberculosis under nutrient starvation
| PRJEB37021 | ENA
Project description:Ribosome profiling provides an opportunity to not only assess how the relative abundance of ribosome association with mRNAs changes in different conditions, but to look more closely at where along mRNAs those ribosomes bind. Here, we used ribosome profiling to calculate the ribosome polarity scores and changes in ribosome footprint read density in both aggregate and gene-specific ways. We profiled a time course of acute glucose starvation followed by glucose readdition and a multi-day growth course through the diauxic shift into stationary phase. We found that ribosome polarity became positive in postdiauxic shift conditions relative to log phase. In acute starvation, polarity shifted positive at our earliest time points but did not continue to do so at later time points. This is consistent with a read density analysis which demonstrated increased density on the 3’ half of genes after glucose starvation. Additionally, we performed ribosome profiling in samples that had glucose added back following acute starvation and observed a wave of new ribosome movement near the start codon and approximately 2,000 nucleotides downstream on open reading frames after one and five minutes of readdition, respectively. Our ribosome profiling analysis suggested that elongation slows during starvation which leads to a buildup of ribosomes on the 3’ halves of mRNAs. Further, it also indicated ribosomes previously built up can resume translation upon glucose readdition. We used reporter assays to corroborate these findings in vivo. Together, these results demonstrate how yeast regulate translation in response to glucose starvation.
2022-04-11 | GSE200491 | GEO
Project description:We used Ribo-seq to examine the effect of Myc activation on protein translation in U2OS cells and correalted these changes with alterations in RNA level measured by RNA-seq on tye same conditions. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR We measure ribosome occupancy profiles in U2OS cells containing an inducible Myc expression vector that were induced or mock-treated in duplicates for 36 hours. In addition, we repeated the experiments in the presence of Torin-1, an inhibitor of mTOR.
2015-11-04 | E-GEOD-66927 | biostudies-arrayexpress
Project description:A universal feature of the response to stress and nutrient limitation is transcriptional upregulation of genes encoding proteins important for survival. Interestingly, under many of these conditions overall protein synthesis levels are reduced, thereby dampening the stress response at the level of protein expression. For example, during glucose starvation in yeast, translation is rapidly and reversibly repressed, yet transcription of many stress- and glucose-repressed genes is increased. Using ribosome profiling and microscopy, we found that this transcriptionally upregulated gene set consists of two classes: (1) one producing mRNAs that are preferentially translated during glucose limitation and are diffusely localized in the cytoplasm – this class includes many heat shock protein mRNAs; and (2) another producing mRNAs that are poorly translated during glucose limitation, have high rates of translation initiation, and are concentrated in foci that co-localize with P bodies and stress granules – this class is enriched for glucose metabolism mRNAs. Remarkably, the information specifying differential localization and translation of these two classes of mRNAs is encoded in the promoter sequence – promoter responsiveness to heat shock factor (Hsf1) specifies diffuse cytoplasmic localization and preferential translation upon glucose starvation, whereas different promoter elements upstream of genes encoding poorly translated glucose metabolism mRNAs direct these mRNAs to RNA granules under glucose starvation. Thus, promoter sequences and transcription factor binding can influence not only mRNA levels, but also subcellular localization of mRNAs and the efficiency with which they are translated, enabling cells to tailor protein production to environmental conditions. Examination of mRNA translation in S. cerevisiae upon glucose starvation.
2014-07-28 | E-GEOD-56622 | biostudies-arrayexpress
Project description:Glutamine addiction represents a metabolic vulnerability of cancer cells although effective therapeutic targeting of the pathways involved remains to be realized. Here, we disclose the critical role of IFRD1 (interferon-related developmental regulator 1) in the adaptive survival of hepatocellular carcinoma cells (HCC) during glutamine starvation. The induction and translocation of IFRD1 to the endoplasmic reticulum inhibits autophagy by promoting proteasomal degradation of the key autophagy regulator ATG14 in a TRIM21-dependent manner. On the contrary, enforced IFRD1 loss increases autophagy flux leading to cell death. This effect is largely realized through the autophagy-dependent degradation of histone H1.0 causing globally enhanced chromatin accessibility associated with unchecked increases in ribosome and protein biosynthesis . This in turn leads to metabolic exhaustion and death under glutamine starvation. Practically, IFRD1 depletion in preclinical HCC models potentiates glutamine limiting strategies including synergizing with the glutaminase-1 selective inhibitor CB-839. Thus, IFRD1 supports the adaptive survival of cancer cells under glutamine starvation, with potential as a therapeutic target in anti-cancer applications.
2024-03-23 | GSE217406 | GEO