Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing analysis of differential expression in supt16h mutants

ABSTRACT: RNA-sequencing analysis of differential expression in supt16h mutants

PROVIDER: PRJNA524919 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8647260_1.fastq.gz	Fastqsanger.gz
	SRR8647260_2.fastq.gz	Fastqsanger.gz
	SRR8647261_1.fastq.gz	Fastqsanger.gz
	SRR8647261_2.fastq.gz	Fastqsanger.gz
	SRR8647262_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA-sequencing analysis of differential expression in supt16h mutants

Project description:Haematopoietic stem cells (HSCs) have long been the focus of developmental and regenerative studies, yet our understanding of the signalling events regulating their specification remains incomplete. We demonstrate that supt16h, a component of the FAcilitates Chromatin Transcription (FACT) complex, is required for HSC formation. Zebrafish supt16h mutants express reduced levels of Notch signalling components, genes essential for HSC development, due to abrogated transcription. Classically, Supt16h regulates transcription and nucleosome reorganization. Whereas global chromatin accessibility in supt16h mutants is unaffected, we observe a specific increase in accessibility at the p53 locus, causing an accumulation of p53 mRNA and protein. We further demonstrate that P53 levels directly influence expression of the Polycomb Group protein, phc1, which functions as a transcriptional repressor of Notch genes. Suppression of phc1 or its upstream regulator, p53, rescues both loss of Notch and loss of HSC phenotypes in supt16h mutants. Taken together, our results highlight a previously uncharacterized relationship between supt16h, p53, and phc1 to specify HSCs via modulation of Notch signalling.

2020-09-01 | GSE127555 | GEO

P53 based ChIP-sequencing of wildtype and mutant supt16h-/- zebrafish

Project description:Hematopoietic stem cells (HSCs) have long been the focus of developmental and regenerative studies, yet our understanding of the signaling events regulating their specification remains incomplete. We demonstrate that supt16h, a component of the FAcilitates Chromatin Transcription (FACT) complex, is required for HSC formation. Zebrafish supt16h mutants express reduced levels of Notch signaling components, genes essential for HSC development, due to abrogated transcription. Classically, Supt16h regulates transcription and nucleosome reorganization. Whereas global chromatin accessibility in supt16h mutants is unaffected, we observe a specific increase in accessibility at the p53 locus, causing an accumulation of p53 mRNA and protein. We further demonstrate that P53 levels directly influence expression of the Polycomb Group protein, phc1, which functions as a transcriptional repressor of Notch genes. Suppression of phc1 or its upstream regulator, p53, rescues both loss of Notch and loss of HSC phenotypes in supt16h mutants. Taken together, our results highlight a previously uncharacterized relationship between supt16h, p53, and phc1 to specify HSCs via modulation of Notch signaling.

2020-09-01 | GSE116088 | GEO

RNA-sequencing based linkage analysis identifies supt16h as a target gene from a forward genetic screen

Project description:Chromatin organization and accessibility are fundamental to how genes are transcriptionally controlled. We identify the first vertebrate mutant for supt16h, a component of the FACT (FAcilitates Chromatin Transcription) complex along with Ssrp1 known to reorganize nucleosomes and assist in transcriptional elongation. We demonstrate its importance in hematopoietic stem cell (HSC) specification by regulating the elongation of Notch genes. Unexpectedly, Assay for Transposase Accessible Chromatin (ATAC) sequencing revealed that loss of supt16h does not affect histone accessibility on a Notch-specific or global level. Although the majority of genes are unaffected, loss of supt16h alters chromatin accessibility significantly at the p53 locus, leading to its overexpression in mutants. Upon downregulation of p53, both loss of Notch and loss of HSC phenotypes are rescued. Notably, ssrp1 mutants possessed normal elongation of Notch genes, levels of P53, and specification of HSCs. Our results highlight the discrete effects of Supt16h and Ssrp1 during HSC specification. Additionally, we demonstrate the relationship between supt16h and p53 during transcriptional elongation to specify HSC fate via modulation of Notch signaling.

2020-09-01 | GSE106342 | GEO

Comparative chromatin accessibility profiling of wildtype and supt16h-/- zebrafish using ATAC-sequencing

2020-09-01 | GSE106341 | GEO

Analysis of differential gene expression in Drosophila dIME4 null mutants

Project description:Analysis of differential gene expression in Drosophila dIME4 null mutants

| PRJNA314696 | ENA

Genome-wide DNA accessibility maps and differential gene expression using ChIP-seq, ATAC-seq and RNA-seq for the human secondary fibroblast cell line hiF-T and whole worms with and without knockdown of FACT complex

Project description:To assess the mechanisms by which FACT depletion leads to increased sensitivity of cells to be reprogrammed, we measured the chromatin accessibility landscape using ATAC-seq following mock treatment, SSRP1 knockdown, or SUPT16H knockdown in human fibroblasts and mock, hmg-3 or hmg-4 knockdown in whole worms, and differential gene expression in hmg-3 knockout mutants or following mock, hmg-4, or spt-16 knockdown by RNAseq.

2018-08-29 | GSE98758 | GEO

Single-Cell RNA-Sequencing: Assessment of Differential Expression Analysis Methods.

Project description:The sequencing of the transcriptomes of single-cells, or single-cell RNA-sequencing, has now become the dominant technology for the identification of novel cell types and for the study of stochastic gene expression. In recent years, various tools for analyzing single-cell RNA-sequencing data have been proposed, many of them with the purpose of performing differentially expression analysis. In this work, we compare four different tools for single-cell RNA-sequencing differential expression, together with two popular methods originally developed for the analysis of bulk RNA-sequencing data, but largely applied to single-cell data. We discuss results obtained on two real and one synthetic dataset, along with considerations about the perspectives of single-cell differential expression analysis. In particular, we explore the methods performance in four different scenarios, mimicking different unimodal or bimodal distributions of the data, as characteristic of single-cell transcriptomics. We observed marked differences between the selected methods in terms of precision and recall, the number of detected differentially expressed genes and the overall performance. Globally, the results obtained in our study suggest that is difficult to identify a best performing tool and that efforts are needed to improve the methodologies for single-cell RNA-sequencing data analysis and gain better accuracy of results.

| S-EPMC5440469 | biostudies-literature

P53 based ChIP-sequencing of wildtype and mutant supt16h-/- zebrafish

Project description:P53 based ChIP-sequencing of wildtype and mutant supt16h-/- zebrafish

| PRJNA476997 | ENA

RNA-seq differential expression analysis of tmRNA (ssrA) mutants in the genome-reduced bacterium Mycoplasma pneumoniae

Project description:We used a combination of genetic and proteomic approaches to characterize tmRNA (ssrA) activity in the genome-reduced bacterium Mycoplasma pneumoniae. For this, we generated tmRNA mutants encoding a tag resistant to proteolysis. Endogenous protein tagging by the mutant tmRNA gene (ssrAmk) was then examined by immunoprecipitation (IP) enrichment followed by LC-MS/MS analysis. Additionally, RNA-seq differential expression analysis of the mutants compared to the wild-type strain was assessed.

2021-08-09 | E-MTAB-10111 | biostudies-arrayexpress

RNA-seq differential expression analysis of tmRNA (ssrA) mutants in the genome-reduced bacterium Mycoplasma pneumoniae

Project description:RNA-seq differential expression analysis of tmRNA (ssrA) mutants in the genome-reduced bacterium Mycoplasma pneumoniae

| PRJEB43137 | ENA