Effect of depletion of Drosophila Hepatocyte Nuclear Factor 4 (dHNF4) in enterocytes on gene expression in the adult midgut
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ABSTRACT:
PROVIDER: PRJNA1133025 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29760640_1.fastq.gz | Fastqsanger.gz | |||
| SRR29760640_2.fastq.gz | Fastqsanger.gz | |||
| SRR29760641_1.fastq.gz | Fastqsanger.gz | |||
| SRR29760641_2.fastq.gz | Fastqsanger.gz | |||
| SRR29760642_1.fastq.gz | Fastqsanger.gz |
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Project description:The main objective of the sudy was to characterize the functions of Drosophila Hepatocyte Nuclear Factor 4 (dHNF4) in midgut enterocytes. For this, we expressed a UAS-dHNF4 RNAi transgene under the control of mex-GAL4, which is active specifically in midgut enterocytes. We then collected adult male midguts, extracted total RNA and performed mRNA-seq. Our data demonstrate that dHNF4 acts as a master regulator of intestinal lipid metabolism in Drosophila.
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Project description:A hallmark of aging-related disease such as neurodegeneration, metabolic disorders, and cancer is the inability of differentiated cells to maintain their identity. In a search for identity regulators, we found that transcription factor Hey supervises the identity of differentiated enterocytes (ECs) in the adult Drosophila midgut. Lineage tracing of ECs established that Hey-deficient ECs lose differentiated identity, are unable to maintain their unique nuclear organization, and exhibit pathological reprograming. Orchestrating this organization, Hey specifies and maintains enhancer activity and nuclear lamins expression, remodeling nuclear architecture from a stem-cell configuration into a differentiated one. Moreover, maintaining this configuration of nuclear lamins is key for cell identity, and lamin misexpression overrides cell identities. At the tissue level, loss of Hey or expression of stem cell-related lamin (LamDm0) in ECs resulted in mis-differentiation, impaired epithelial integrity, and reduced organismal survival. Thus, a single transcription factor concomitantly supervises chromatin and nuclear organization, safeguarding cell identity
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Project description:Hepatocyte nuclear factor 1β binding in E14.5 kidney
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Project description:Background and Aims: Hepatocyte nuclear factor 1 (HNF1) transcription factors direct tissue specific gene regulation in liver, pancreas and kidney and are associated with diabetes. Here we investigate the transcriptional network governed by HNF1 in an intestinal epithelial cell line. Methods: Chromatin immunoprecipitation followed by direct sequencing (ChIP-seq) was used to identify HNF1 binding sites genome-wide. Direct targets of HNF1 were validated using conventional ChIP assays. siRNA-mediated depletion of HNF1 followed by RT-qPCR further confirmed target genes. The effect of HNF1 reduction on glucose uptake was measured by fluorescence activated cell sorting (FACS) following treatment of intestinal epithelial cells with 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-d-glucose (2-NBDG, a fluorescent glucose mimic). Results: HNF1 controls multiple pathways that are critical for intestinal epithelial cell function, including properties of the cell membrane, cellular response to hormones, and regulation of biosynthetic processes. Approximately 50% of HNF1 binding sites are also occupied by hepatocyte nuclear factor 4A (HNF4A), caudal type homeobox 2 (CDX2), and forkhead box A2 (FOXA2). Depletion of HNF1 increases FOXA2 abundance and decreases levels of CDX2. Moreover, loss of HNF1 inhibits glucose uptake by the intestinal epithelial cell line. Conclusions: These data show that HNF1 plays a critical role in regulating intestinal epithelial cell functions including glucose absorption. HNF1 interacts with other tissue-specific transcription factors to regulate differentiated properties of these cells.
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Project description:A midgut reference sample is compared to midgut samples taken at various stages before (18h, 4h), at (0h), and after (2h, 3h, 4h, 5h, 6h, 8h, 10h, 12h) puparium formation. Keywords = Drosophila, ecdysone, network, genomic, microarray, organogenesis, EcR, midgut, central nervous system, salivary gland, epidermis, imaginal disc, development Keywords: other
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Project description:Aedes aegypti mosquito, vector for several viral diseases, undergoes significant physiological changes after a blood meal. Through single-cell RNA sequencing and metabolomics, we unveiled dynamic cellular composition and metabolic adaptations within abdominal midgut and fat body tissues. We revealed high cell diversity, specialized in digestion, metabolism, immunity, and reproduction. While the midgut primarily comprises enterocytes, enteroendocrine, cardia and intestinal stem cells, the fat body consists of not only trophocytes and oenocytes, but also a substantial population of hemocytes and fat body-yolk cells (FYC). The fat body, exhibiting a more complex metabolomic profile than the midgut, played a central role in immune and metabolic gene expression, particularly within trophocytes and FYCs. Additionally, insect-specific viruses were detected at the single-cell level, mainly in the midgut at later stages post-blood meal. These findings offer new vector control strategies by targeting specific abdominal cell populations and metabolic pathways involved after a blood meal.
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Project description:Comparisons between EcR mutant midgut and a reference control sample from mixed-stage normal midgut Keywords = Drosophila, ecdysone, network, genomic, microarray, organogenesis, EcR, midgut, central nervous system, salivary gland, epidermis, imaginal disc, development Keywords: other
2003-07-23 | GSE540 | GEO
Project description:Digested dietary fats are taken up, processed and transported by enterocytes to supply the body with lipids. Most absorbed lipids are assembled into pre-chylomicrons in the endoplasmic reticulum (ER) of enterocytes, which are then transported to the Golgi for maturation and subsequent secretion to the circulation. The role of mitochondria in regulating intestinal lipid transport remains unknown. Here we show that mitochondrial dysfunction in enterocytes inhibits chylomicron production and the transport of dietary lipids to peripheral organs. Mice with intestinal epithelial cell (IEC)-specific ablation of the mitochondrial-specific aspartyl - tRNA synthetase DARS2, as well as of the respiratory chain subunit SDHA or the assembly factor COX10 failed to thrive and showed massive accumulation of lipids within large lipid droplets (LDs) in enterocytes of the proximal small intestine (SI). Feeding a fat-free diet inhibited the formation of LDs in DARS2-deficient enterocytes, showing that accumulating lipids derive mostly from digested fat. Furthermore, metabolic tracing studies revealed impaired transport of dietary lipids to peripheral organs in mice lacking DARS2 in IECs. Moreover, DARS2-deficient enterocytes showed a distinct lack of mature chylomicrons concomitant with a disorganisation of the Golgi apparatus, suggesting that impaired ER to Golgi trafficking underlies impaired chylomicron production and secretion. Taken together, these results revealed a vital role of mitochondria in regulating dietary lipid transport in enterocytes, which is relevant for understanding the intestinal and nutritional defects observed in patients with mitochondrial defects.
2023-12-21 | PXD026934 | Pride
Project description:Hepatocyte nuclear factor-4α (HNF4α, NR2A1) is a nuclear receptor which has a critical role in hepatocyte differentiation and the maintenance of homeostasis in the adult liver. However, a detailed understanding of native HNF4α in the steady state remains to be elucidated. Here we report the native HNF4α isoforms, phosphorylation status and complexes in the steady state, as shown by shotgun proteomics in HepG2 hepatocarcinoma cells. Shotgun proteomic analysis revealed the complexity of native HNF4α, including multiple phosphorylation sites and inter-isoform heterodimerization. The associating complexes identified by label-free semi-quantitative proteomic analysis include the following: the DNA-dependent protein kinase catalytic subunit, histone acetyltransferase complexes, mRNA splicing complex, other nuclear receptor coactivator complexes, the chromatin remodeling complex, and the nucleosome remodeling and histone deacetylation complex. Among the associating proteins, GRB10 interacting GYF protein 2 (GIGYF2, PERQ2) is a new candidate cofactor in metabolic regulation. Moreover, an unexpected heterodimerization of HNF4α and Hepatocyte nuclear factor-4γ was found. A biochemical and genome-wide analysis of transcriptional regulation showed that this heterodimerization activates gene transcription. The genes thus transcribed include the cell death-inducing DEF45-like effector b (CIDEB) gene, which is an important regulator of lipid metabolism in the liver. This suggests that the analysis of the distinctive stoichiometric balance of native HNF4α and its cofactor complexes described here is important for an accurate understanding of transcriptional regulation. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.
2010-12-22 | E-GEOD-18990 | biostudies-arrayexpress