Time series mRNA abundance measurement triggered by ActinomycinD treatment in patient iPSC derived neurons
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE199349 | GEO | 2022/06/01
REPOSITORIES: GEO
Similar Datasets
Project description:Time series mRNA abundance measurement triggered by ActinomycinD treatment in patient iPSC derived neurons
| PRJNA819434 | ENA
Project description:whole embryo (all tissues) measurement of mRNA decay by 4-thiouridine pulse-chase These TU-Decay microarrays analyze mRNA levels at three timepoints: a one hour pulse, one hour chase, and three hour chase. Measurements with or without transcription inhibition by actinomycin D (ActD) were compared.
2015-03-31 | E-GEOD-67435 | biostudies-arrayexpress
Project description:To investigate the potential influence of transcription on mRNA stability in mammalian cells, we tested the global relationship between rates of synthesis and decay of mRNAs. We estimated synthesis rates by flash 4sU labeling followed by RNA-seq, and decay rates by treating cells with Actinomycin D (ActD) for 0, 2, 4 and 6 hours and measuring half-lives of all expressed genes by MARS-seq analysis. As short-term perturbations of transcription elongation dynamics diminished mRNA stability, we next wished to examine the effect of extended transcription slowdown. To this end, we treated cells with CPT for 24 hours and profiled mRNA stability in a genome-wide manner using ActD time-course and MARS-seq.
2020-03-10 | GSE145097 | GEO
Project description:The study aims to investigate functions of PfNOT1.1 in regulating mRNA decay in the malaria parasite, P. falciparum. To achieve this goal, transcription was blocked by actinomycin D (actD) and the transcriptional profilling of parasites was analyzed by microarray technology.
2021-08-31 | GSE142527 | GEO
Project description:The goal of this study is to measure Arabidopsis mRNA transcription and mRNA decay rates genome wide at two temperatures, and thus to calculate the temperature coefficient of both processes. Sensing and response to ambient temperature is important for controlling growth and development of many organisms, in part by regulating mRNA levels. mRNA abundance can change with temperature, but it is unclear whether this results from changes to transcription or decay rates and whether passive or active temperature regulation is involved. Results Using a base analogue labelling method we directly measured the temperature coefficient (Q10) of mRNA synthesis and degradation rates of the Arabidopsis transcriptome. We show that for most genes transcript levels are buffered against passive increases in transcription rates by balancing passive increases in the rate of decay. Strikingly, for temperature-responsive transcripts, increasing temperature raises transcript abundance primarily by promoting faster transcription relative to decay and not vice versa, suggesting a global transcriptional mechanism process exists for the activethat controls of mRNA abundance by temperature/
2013-12-07 | GSE53071 | GEO
Project description:The goal of this study is to measure Arabidopsis mRNA transcription and mRNA decay rates genome wide at two temperatures, and thus to calculate the temperature coefficient of both processes. Sensing and response to ambient temperature is important for controlling growth and development of many organisms, in part by regulating mRNA levels. mRNA abundance can change with temperature, but it is unclear whether this results from changes to transcription or decay rates and whether passive or active temperature regulation is involved. Results Using a base analogue labelling method we directly measured the temperature coefficient (Q10) of mRNA synthesis and degradation rates of the Arabidopsis transcriptome. We show that for most genes transcript levels are buffered against passive increases in transcription rates by balancing passive increases in the rate of decay. Strikingly, for temperature-responsive transcripts, increasing temperature raises transcript abundance primarily by promoting faster transcription relative to decay and not vice versa, suggesting a global transcriptional mechanism process exists for the activethat controls of mRNA abundance by temperature/ The design of this expreiment is thus: at time zero (dawn) 3 biological replicate samples were harvested, and then the base analogue 4-thiouracil (4SU) was added to three remaining biological replicate samples. At time T these were harvested and the latter biotinylated and separated into 4SU-containing (labelled) and 4SU non-containing (unlabelled) fractions by passage through a streptavidin column. Total RNA for both timepoints was hybridisaed on the chips, as were the separated fractions from time T, giving 12 chips in total. This design was repeated at a second temperature, giving 24 hybridisations. The two tempertaures were 27C and 17C and time T was 1 hour after dawn at 27C and two hours after dawn at 17C.
2013-12-07 | E-GEOD-53071 | biostudies-arrayexpress
Project description:For each strain two time courses for mRNA abundance: Oxidative and MMS and two time courses for decay: reference decay and following oxidative stress
2011-07-30 | GSE26829 | GEO
Project description:For each strain two time courses for mRNA abundance: Oxidative and MMS and two time courses for decay: reference decay and following oxidative stress We used Affymetrix microarrays to quantify changes in mRNA abundance following oxidative stress and DNA damage stress and also decay following transcription inhibition with and without oxidative stress. Each of the experiments were done for both strains 211 (wt) and 212 (mutant)
2011-07-29 | E-GEOD-26829 | biostudies-arrayexpress
Project description:The naïve pluripotent epiblast cells become polarized into a rosette-like structure, followed by irreversible transition into primed pluripotency during one of the fastest morphological switches termed lumenogenesis. This requires rapid decay of pluripotency-associated mRNAs, but the underlying mechanism remains unknown. Guided by machine learning and metabolic RNA sequencing, we identified RNA binding proteins (RBPs), especially LIN28A, as primary mRNA decay factors. To understand if RBP dynamics steer embryogenesis, we used mRNA-RBP interactome capture during naïve-rosette-epiblast-gastrulation progression. We identified a dramatic increase in LIN28A mRNA binding, driven by its nucleolus-to-cytoplasm translocation during the naïve-primed pluripotency transition. Cytoplasmic LIN28A binds to 3’UTRs of pluripotency-associated mRNAs to directly stimulate their decay, and thereby progression to lumenogenesis. Accordingly, forced nuclear retention of LIN28A impeded lumenogenesis, causing an unforeseen embryonic multiplication and impaired gastrulation. This reveals selective mRNA decay, driven by nucleo-cytoplasmic RBP translocation, as an intrinsic mechanism for cell identity switch that controls embryonic timing of lumenogenesis.
2024-03-01 | GSE169547 | GEO
Project description:The naïve pluripotent epiblast cells become polarized into a rosette-like structure, followed by irreversible transition into primed pluripotency during one of the fastest morphological switches termed lumenogenesis. This requires rapid decay of pluripotency-associated mRNAs, but the underlying mechanism remains unknown. Guided by machine learning and metabolic RNA sequencing, we identified RNA binding proteins (RBPs), especially LIN28A, as primary mRNA decay factors. To understand if RBP dynamics steer embryogenesis, we used mRNA-RBP interactome capture during naïve-rosette-epiblast-gastrulation progression. We identified a dramatic increase in LIN28A mRNA binding, driven by its nucleolus-to-cytoplasm translocation during the naïve-primed pluripotency transition. Cytoplasmic LIN28A binds to 3’UTRs of pluripotency-associated mRNAs to directly stimulate their decay, and thereby progression to lumenogenesis. Accordingly, forced nuclear retention of LIN28A impeded lumenogenesis, causing an unforeseen embryonic multiplication and impaired gastrulation. This reveals selective mRNA decay, driven by nucleo-cytoplasmic RBP translocation, as an intrinsic mechanism for cell identity switch that controls embryonic timing of lumenogenesis.
2024-03-01 | GSE169549 | GEO