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Transcriptomic analysis of the liver from control sibling and mutant uhrf1-hi272 zebrafish larvae at 120 hpf treated with DMSO or Palbociclib (PD)

ABSTRACT: Transcriptomic analysis of the liver from control sibling and mutant uhrf1-hi272 zebrafish larvae at 120 hpf treated with DMSO or Palbociclib (PD)

PROVIDER: PRJNA983848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24921906_1.fastq.gz	Fastqsanger.gz
	SRR24921906_2.fastq.gz	Fastqsanger.gz
	SRR24921907_1.fastq.gz	Fastqsanger.gz
	SRR24921907_2.fastq.gz	Fastqsanger.gz
	SRR24921908_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of the liver from control sibling and mutant uhrf1-hi272 zebrafish larvae at 120 hpf treated with DMSO or Palbociclib (PD)

Project description:This study was carried out to compare the changes in gene expression in livers of 120 hpf control sibling and mutant uhrf1-hi272 zebrafish larvae in response to treatment with DMSO or Palbociclib (PD)

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RNA-Seq of 120 hpf control sibling and mutant uhrf1 hi272 zebrafish livers

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RNA-Seq of 120 hpf control sibling and mutant uhrf1 hi272 zebrafish livers

Project description:RNA-Seq of 120 hpf control sibling and mutant uhrf1 hi272 zebrafish livers

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Comparing the genome-wide chromatin accessibility of uhrf1 hi272 mutants and phenotypically wildtype whole zebrafish embryos at 120 hpf using ATAC-Seq.

Project description:The goal of this study is to study the chromatin accessibility differences between control and uhrf1 hi272 mutant 120 hpf zebrafish embryos (uhrf1 hi272+/-, Tg(fabp10a:CAAX-EGFP) using ATAC-Seq technique.

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Genome-wide chromatin accessibility and DNA methylation of wildtype zebrafish livers at 120 hpf

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Transcriptomic profiling of the liver from dnmt1 mutant zebrafish larvae compared to their phenotypically normal siblings at 120 hpf

Project description:In this dataset we performed RNA-seq on pools of livers dissected at 120 hpf from dnmt1(s904) mutants and phenotipically wild-type looking siblings.

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Genome-wide expression profiling of whole of uhrf1 mutant zebrafish compared to WT siblings at 120 hpf

Project description:The goal of this study is to compare gene expression levels in whole uhrf1 mutant larvae to phenotypically normal siblings.

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Differential gene expression in the liver of zebrafish larvae exposed to 1 mM inorganic arsenic from 4-120 hpf

Project description:The goal of this study is to compare gene expression levels in the livers of larval Tg(fabp10:nls-mcherry) exposed to 1 mM inorganic arsenic from 4-120 hpf to the unexposed siblings. Samples were collected from Tg(fabp10:nls-mcherry) zebrafish larvae that were derived from incrossed parents of the same strain. The background of transgenic lines were typically from mixed outcrosses of the transgenics to AB, TAB5, and TAB14 strains when regenerating the lines as the working stocks aged. All samples were collected at approximately 120 hpf - natural spawning at 8:30-9:00AM EST on day zero, samples were collected at 8-10AM EST on day 5.

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Transcriptomic profiling of whole larvae and the liver from dnmt1 mutant zebrafish larvae compared to their phenotypically normal siblings at 120 hpf

Project description:This SuperSeries is composed of the SubSeries listed below which has both RNAseq (from whole larvae and pools of dissected livers) and methylome profiling using reduced representation bisulfite sequencing (from whole larvae) at 120 hours post-fertilization (hpf).

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Gene expression profiles of uhrf1 mutant zebrafish

Project description:UHRF1 (Ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemimethylated DNA during replication, is essential for maintaining DNA methylation patterns during cell division and is suggested to direct additional repressive epigenetic marks. Uhrf1 mutation in zebrafish results in multiple embryonic defects including failed hepatic outgrowth, but the epigenetic basis of these phenotypes is not known. We find that DNA methylation is the only epigenetic mark that is depleted in uhrf1 mutants and make the surprising finding that despite the reduced organ size in uhrf1 mutants, genes regulating DNA replication and S-phase progression were highly upregulated. Further, there is a striking increase in BrdU incorporation in uhrf1 mutant cells, and they retained BrdU labeling over several days, indicating they are arrested in S-phase. Moreover, some of the label retaining nuclei co-localized with TUNEL positive nuclei, suggesting that arrested cells are responsible for apoptosis. Importantly, dnmt1 mutation phenocopies the S-phase arrest and hepatic outgrowth defects in uhrf1 mutants and Dnmt1 knock-down enhances the uhrf1 hepatic phenotype. Together, these data indicate that DNA hypomethylation is sufficient to generate the uhrf1 mutant phenotype by promoting an S-phase arrest. We thus propose that cell cycle arrest is a mechanism to restrict propagation of epigenetically deranged cells during embryogenesis. Genome-wide expression profiling was performed on 2 uhrf1 mutant and 2 wildtype zebrafish larvae (120 hours post fertilization) by using Zebrafish Genome Array (Affymetrix) according to manufacturer's instruction.

2015-02-09 | E-GEOD-55339 | biostudies-arrayexpress

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