Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genetic roles of Hnf4 family transcription factors in zebrafish development and microbial response

ABSTRACT: The goal of this study was to better understand the roles of Hnf4 fmaily transcription factors in zebrafish development and intestinal function. We used RNA-sequencing to compare gene expression changes in digestive tracts dissected from 6dpf larval zebrafish. Our first experiment compared samples from wild type and hnf4g-/- zebrafish which were either raised germ free or with a conventional microbiota starting at 3dpf. The second experiment compared samples from wild type, hnf4g-/-, and hnf4a-/-;hnf4g-/- zebrafish conventionally raised from 0dpf with a microbiota. Each sample consists of RNA extracted from 10-15 pooled gastrointestinal tracts, and 4 biological replicates per treatment group were sequenced.

ORGANISM(S): Danio rerio

PROVIDER: GSE183799 | GEO | 2022/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Zebrafish response to microbiota

2010-01-01 | GSE16857 | GEO

Transcriptional and chromatin profiles of duodenum epithelium upon HNF4 loss in mice by RNA-seq and ChIP-seq

Project description:We find that HNF4G is an intestine-particular HNF4 paralog, and works redundantly with HNF4A for driving intestinal differentiation by controlling chromatin accessibility and regulating thousands of transcripts particular to differentiated cells. Without HNF4s, cells fail to achieve a differentiated state. A positive feedback loop between HNF4 transcriptional regulation and BMP/SMAD signaling stabilizes differentiation, and the two inputs cooperatively activate differentiation gene expression.

2019-04-08 | GSE112946 | GEO

Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha (zebrafish RNA-seq)

Project description:We performed RNA-seq from 6 days post fertilization hnf4a-/- and hnf4a+/+ zebrafish larval digestive tracts raised in the absence (Germ Free, GF) or presence (Conventionalized, CV) of microbiota. We found that zebrafish hnf4a activates almost half of the microbiota-suppressed genes, indicating that the microbiota supress Hnf4a trans-activity. We also provide evidence suggesting that microbial suppression of Hnf4a may contribute to IBD pathogenesis.

2017-03-27 | GSE90446 | GEO

Zebrafish response to microbiota

Project description:Vertebrates are colonized at birth by complex microbial communities (microbiota) that influence diverse aspects of host biology. We have used a functional genomics approach to identify zebrafish genes that are differentially expressed in response to the microbiota. We assessed RNA expression profiles from zebrafish larvae at 6 days post-fertilization (dpf) that were either raised continuously in the absence of any microorganism (germ-free or GF), or raised GF through 3dpf then colonized with a normal zebrafish microbiota (conventionalized or CONVD). Total RNA was purified from pooled intact zebrafish larvae (28-80 larvae/pool, 3 biological replicate pools/condition) using Trizol reagent (Invitrogen) followed by DNase I digestion (DNA-Free, Ambion) according to manufacturers' protocols. Total RNA from each replicate pool (12ug RNA/replicate) was used as template for independent cDNA synthesis and in vitro transcription reactions (BioArray HighYield RNA Transcript Labeling Kit; Enzo Life Sciences) to generate biotinylated cRNA targets. cRNA targets (20ug/replicate) were fragmented using standard methods. Hybridization and scanning were performed using standard Affymetrix protocol. Raw expression values were normalized (Invariant set method) and modeled (PM-MM model), and present/absent calls were generated using dChip software (build date Dec.11, 2005).

2009-12-31 | E-GEOD-16857 | biostudies-arrayexpress

Transcription profiling of mouse HNF4 null small intestine

Project description:To define changes in gene expression resulting from loss of hnf4 in the small intestine. Experiment Overall Design: hnf4 null intestines were generated by breeding hnf4loxp mice to vill-cre mice. Animals appeared to be healthy. Gene arrays were performed on two null and two control intestines.

2008-06-12 | E-GEOD-3124 | biostudies-arrayexpress

Transcription profiling of mouse HNF4 null mutant colon vs. control colons

Project description:Background and Aims: HNF4? is a nuclear hormone receptor transcription factor that has been shown to be required for hepatocyte differentiation and development of the liver. It has also been implicated in regulating expression of genes that act in the epithelium of the lower gastrointestinal tract. This implied that HNF4? might be required for development of the gut. Methods: We generated mouse embryos in which Hnf4? was ablated in the epithelial cells of the fetal colon using Cre-loxP technology. Embryos were examined using a combination of histology, immunohistochemistry, gene array and RT-PCR, and chromatin immunoprecipitation analyses to define the consequence of loss of HNF4? on colon development. Results: Embryos could be generated until E18.5 that lacked HNF4? in their colon. Although, early stages of colonic development occurred, HNF4? null colons failed to form normal crypts. In addition, goblet cell maturation was perturbed and expression of an array of genes that encode proteins with diverse roles in colon function was disrupted. Several genes whose expression in the colon was dependent on HNF4? contained HNF4?âbinding sites sequences within putative transcriptional regulatory regions and a subset of these sites were occupied by HNF4? in vivo. Conclusion: HNF4? is a transcription factor that is essential for development of the mammalian colon, regulates goblet cell maturation and is required for expression of genes that control normal colon function and epithelial cell differentiation. Experiment Overall Design: COMPARISON OF 3 MUTANT TO 2 CONTROL COLONS.

2008-06-12 | E-GEOD-3116 | biostudies-arrayexpress

HNF4 small intestine knockout

Project description:To define changes in gene expression resulting from loss of hnf4 in the small intestine. Keywords: genetic modification

2005-12-31 | GSE3124 | GEO

3dpf untreated zebrafish larvae vs. 3dpf zebrafish larvae treated with 20mM PTZ for 30 minutes and 90 minutes

Project description:Transcriptional profiling of 3dpf wild type zebrafish larvae treated with 20mM PTZ for 30 and 90 minutes compared with 3dpf wild type control untreated zebrafish larvae.

2017-02-24 | GSE95312 | GEO

Accessible chromatin profiles of intestinal epithelial cells upon HNF4 loss in embryos by ATAC-seq

Project description:HNF4 paralogs are redundantly required for proper villus elongation, differentiation and maturation in the developing gut. We find 5,391 chromatin regions become inaccessible upon HNF4 loss, and HNF4 binding sequences are most enriched in these regions. Genes nearby these 5,391 HNF4 dependent regions are associated with villus differentiation/maturation.

2019-07-29 | GSE128674 | GEO

Expression profiling of HNF4-dependent transcripts in Drosophila larvae

Project description:We show that dHNF4 null mutant larvae are sensitive to starvation. Starved mutant larvae consume glycogen normally, but retain lipids in their midgut and fat body, and have increased levels of long chain fatty acids, suggesting that they are unable to efficiently mobilize stored fat for energy. HNF4 dependent transcripts were identified under fed and starved conditions. Microarray studies indicate reduced expression of genes that control lipid catabolism and beta-oxidation. Late second instar control and HNF4 mutant larvae were collected and fed or starved for 24 hours, and then RNA was isolated for analysis. Taken together, our results support a feed-forward model for dHNF4, in which fatty acids released from triglycerides activate the receptor, inducing enzymes that drive fatty acid oxidation for energy production. Keywords: expression profiling, HNF4, mutants, Affymetrix, Drosophila 2.0, starvation, TAG, fatty acid, beta-oxidation

2009-01-24 | GSE14531 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data