Transciptome profiling of 18 breast cancer cell llines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE152102 | GEO | 2020/06/16
REPOSITORIES: GEO
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Project description:Mature tRNA pools were measured using an adaptation of YAMAT-seq (Shigematsu et al., 2017; doi:10.1093/nar/gkx005 ) and further described in (Ayan et al., 2020; doi:10.7554/eLife.57947) in 10 strain-medium combinations (all strains dervied from the model bacterium E. coli MG1655). The aim of the experiment was to investigate the effect of reducing tRNA gene copy number on mature tRNA pools in rich and poor media.
2022-12-02 | GSE198606 | GEO
Project description:Inactivation of prospero in Drosophila neuroblasts during larval stages induces unlimited neuroblast amplification leading to tumors that persist growing in adults. Tumors present in the ventral nerve cord of adult flies were dissected, dissociated and GFP-labelled tumor neuroblasts were isolated by FACS. 10000 neuroblasts were then processed for single-cell RNA-seq analysis. Single Cell RNA sequencing library were generated using the 10x Genomics Chromium Platform and sequenced on the Illumina Nextseq 500. eLife 2019;8:e50375 DOI: 10.7554/eLife.50375
2019-10-10 | GSE114986 | GEO
Project description:Transciptome profiling of 18 breast cancer cell llines
| PRJNA638351 | ENA
Project description:Mature tRNA pools were measured using an adaptation of YAMAT-seq (Shigematsu et al., 2017; doi:10.1093/nar/gkx005 ) and further described in (Ayan et al., 2020; doi:10.7554/eLife.57947) in eight strains dervied from the model bacterium, Pseudomonas fluorescens SBW25. The aim of the experiment was to determine the effect on the mature tRNA pool of (i) removing multi-copy tRNA genes by genetic engineering, and (ii) duplicating tRNA genes during a subsequent, compensatory evolution experiment. We found that (i) results in a reduction in some tRNA isotypes in the mature tRNA pool, and (ii) results in an increase in a compensatory increase in their expression.
2022-12-02 | GSE196705 | GEO
Project description:ISWI-family nucleosome remodeling enzymes need the histone H4 N-terminal tail to mobilize nucleosomes. Here we mapped the H4-tail binding pocket of ISWI. Surprisingly the binding site was adjacent to but not overlapping with the docking site of an auto-regulatory motif, AutoN, in the N-terminal region (NTR) of ISWI, indicating that AutoN does not act as a simple pseudosubstrate as suggested previously. Rather, AutoN cooperated with a hitherto uncharacterized motif, termed AcidicN, to confer H4-tail sensitivity and discriminate between DNA and nucleosomes. A third motif in the NTR, ppHSA, was functionally required in vivo and provided structural stability by clamping the NTR to Lobe 2 of the ATPase domain. This configuration is reminiscent of Chd1 even though Chd1 contains an unrelated NTR. Our results shed light on the intricate structural and functional regulation of ISWI by the NTR and uncover surprising parallels with Chd1. Elife. 2017 Jan 21;6. pii: e21477. doi: 10.7554/eLife.21477. [Epub ahead of print]
2017-02-02 | PXD005831 | Pride
Project description:Genetic and molecular approaches have been critical for elucidating the mechanism of the mammalian circadian clock. Here, we demonstrate that the ClockM-NM-^T19 mutant behavioral phenotype is significantly modified by mouse strain genetic background. We map a suppressor of the ClockM-NM-^T19 mutation to a M-bM-^HM-<900 kb interval on mouse chromosome 1 and identify the transcription factor, Usf1, as the responsible gene. A SNP in the promoter of Usf1 causes elevation of its transcript and protein in strains that suppress the Clock mutant phenotype. USF1 competes with the CLOCK:BMAL1 complex for binding to E-box sites in target genes. Saturation binding experiments demonstrate reduced affinity of the CLOCKM-NM-^T19:BMAL1 complex for E-box sites, thereby permitting increased USF1 occupancy on a genome-wide basis. We propose that USF1 is an important modulator of molecular and behavioral circadian rhythms in mammals. DOI:http://dx.doi.org/10.7554/eLife.00426.001. Examination of 3 transcriptional regulators in mouse liver at ZT8
2013-04-21 | E-GEOD-44609 | biostudies-arrayexpress
Project description:We generated induced excitatory sensory neurons (iNeurons, iNs) from pluripotent stem cells of great apes (Human, Chimpanzee and Bonobo) by expressing the transcription factor neurogenin 2 (Ngn2). Single cell-RNA sequencing was performed to identify gene expressions differing in dendrite and synapse development during iNs maturation. Briefly, cultured cells were first dissociated and yield a concentration of 500 to 1000 cells/ml to obtain approximately 3000 cells per lane of a 10X microfluidic chip device. Single cell gene expression libraries were generated using the 10X Chromium Single Cell 3’ v2 Kit following the manufacturer’s instructions. Quantification and quality control of libraries was performed using a High Sensitivity DNA chip for Agilent’s Bioanalyzer and sequenced on a HiSeq2500 in Rapid sequencing mode. Our single-cell RNA-Seq data can be explored using our ShinyApp-based browser called iNeuronExplorer: https://bioinf.eva.mpg.de/shiny/iNeuron_Explorer/ (for details, please see this paper: DOI: 10.7554/eLife.59323). Sequencing raw data for all iNeurons from 409B2 line, one culture of day 35 iNeurons from H9 line and one culture of day 35 iNeurons from SC102A1 line are deposited under Mendeley Data with doi: 10.17632/y3s4hnyvg6, their corresponding gene counts (UMIs) are deposited in this ArrayExpress experiment with accession number MTAB-9233.
2020-12-15 | E-MTAB-9233 | biostudies-arrayexpress
Project description:Genetic and molecular approaches have been critical for elucidating the mechanism of the mammalian circadian clock. Here, we demonstrate that the ClockΔ19 mutant behavioral phenotype is significantly modified by mouse strain genetic background. We map a suppressor of the ClockΔ19 mutation to a ∼900 kb interval on mouse chromosome 1 and identify the transcription factor, Usf1, as the responsible gene. A SNP in the promoter of Usf1 causes elevation of its transcript and protein in strains that suppress the Clock mutant phenotype. USF1 competes with the CLOCK:BMAL1 complex for binding to E-box sites in target genes. Saturation binding experiments demonstrate reduced affinity of the CLOCKΔ19:BMAL1 complex for E-box sites, thereby permitting increased USF1 occupancy on a genome-wide basis. We propose that USF1 is an important modulator of molecular and behavioral circadian rhythms in mammals. DOI:http://dx.doi.org/10.7554/eLife.00426.001.
2013-04-21 | GSE44609 | GEO
Project description:vasc1-bravo-Transciptome of VASC1
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Project description:In embryos, DCC binding across the length of the ~17.7 Mb X chromosome initiates at a set of recruitment elements on the X (rex). Individual rex sites collectively contribute to recruitment and repression, thus deletion of one or few rex sites causes subtle changes, as measured by mRNA-seq in mixed-stage embryos. We previously constructed a strain deleting rex-1, located ~6 kb downstream of dpy-23 (https://doi.org/10.7554/eLife.23645). Here we performed mRNA-seq in rex-1 deletion embryos.
2024-04-29 | GSE265989 | GEO