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Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

ABSTRACT: Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

PROVIDER: PRJNA864065 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20723932_1.fastq.gz	Fastqsanger.gz
	SRR20723932_2.fastq.gz	Fastqsanger.gz
	SRR20723933_1.fastq.gz	Fastqsanger.gz
	SRR20723933_2.fastq.gz	Fastqsanger.gz
	SRR20723934_1.fastq.gz	Fastqsanger.gz

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Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

Project description:Zinc is an essential micronutrient that is believed to influence gut homeostasis by unclear mechanisms. Jimenez et al. identify that zinc transporter Zip14 is essential to maintain protective systems, lower inflammation, and limit dysbiosis through mechanisms that control histone deacetylase activity and transcription factor occupancy of specific genes in intestinal epithelial cells.

2022-12-14 | GSE210160 | GEO

Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms.

Project description:Zinc has anti-inflammatory properties using mechanisms that are unclear. Zip14 (Slc39a14) is a zinc transporter induced by proinflammatory stimuli and is highly expressed at the basolateral membrane of intestinal epithelial cells (IECs). Enterocyte-specific Zip14 ablation (Zip14ΔIEC) in mice was developed to study the functions of this transporter in enterocytes. This gene deletion led to increased intestinal permeability, increased IL-6 and IFNγ expression, mild endotoxemia, and intestinal dysbiosis. RNA sequencing was used for transcriptome profiling. These analyses revealed differential expression of specific intestinal proinflammatory and tight junction (TJ) genes. Binding of transcription factors, including NF-κβ, STAT3, and CDX2, to appropriate promoter sites of these genes supports the differential expression shown with chromatin immunoprecipitation assays. Total histone deacetylase (HDAC), and specifically HDAC3, activities were markedly reduced with Zip14 ablation. Intestinal organoids derived from ΔIEC mice display TJ and cytokine gene dysregulation compared with control mice. Differential expression of specific genes was reversed with zinc supplementation of the organoids. We conclude that zinc-dependent HDAC enzymes acquire zinc ions via Zip14-mediated transport and that intestinal integrity is controlled in part through epigenetic modifications.NEW & NOTEWORTHY We show that enterocyte-specific ablation of zinc transporter Zip14 (Slc39a14) results in selective dysbiosis and differential expression of tight junction proteins, claudin 1 and 2, and specific cytokines associated with intestinal inflammation. HDAC activity and zinc uptake are reduced with Zip14 ablation. Using intestinal organoids, the expression defects of claudin 1 and 2 are resolved through zinc supplementation. These novel results suggest that zinc, an essential micronutrient, influences gene expression through epigenetic mechanisms.

| S-EPMC9925170 | biostudies-literature

Masison2024 - Enterocyte Iron Mucosal Block

Project description:Enterocyte Iron Mucosal Block This is a model of enterocyte iron absorption, consisting of iron uptake (movement of iron from intestinal lumen into cytplasm), and transfer (transport of iron from cytoplasm to blood/plasma). The model was created by Joseph Masison and Pedro Mendes. Intestinal mucosal block is a cellular phenomenon defined by a transient reduction in iron absorption by intestinal epithelial cells following previous iron exposures. Understanding what controls the mucosal block is central to understanding how intestinal iron absorption contributes to pathological iron states. Three mechanisms implicated in driving mucosal block are the endocytosis of divalent metal transporter 1 (DMT1), sequestration of iron by cytosolic ferritin, and iron regulatory proteins (IRPs) regulation of ferritin expression. Here, we build a model that reproduces the mucosal block phenomena, based on published experimental data, and use it to quantify the contribution of each mechanism to the block. Model analysis shows ferritin and IRPs regulation have the largest quantitative impact on the mucosal block. Lastly, DMT1 endocytosis is shown to play a role in limiting total enterocyte iron uptake, protecting the cell against oxidative stress, but does not contribute to the decrease in total iron transfer seen in mucosal block. CC0 1.0 Universal: To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission. Please refer to CC0 Public Domain Dedication for more information.

2025-02-11 | MODEL2405170001 | BioModels

Deregulated overexpression of the high affinity Cu transporter COPT1 alters iron homeostasis in Arabidopsis

Project description:Deregulated overexpression of the high affinity Cu transporter COPT1 alters iron homeostasis in Arabidopsis

| PRJNA601916 | ENA

Deletion of Metal Transporter Zip14 (Slc39a14) Reduces Major Histocompatibility Complex II Expression in Murine Small Intestinal Epithelial Cells

Project description:Deletion of Metal Transporter Zip14 (Slc39a14) Reduces Major Histocompatibility Complex II Expression in Murine Small Intestinal Epithelial Cells

| PRJNA1179338 | ENA

Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

Project description:Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

| PRJNA664402 | ENA

RNA-seq analysis of the effect of kanamycin and the ABC transporter AtWBC19 on Arabidopsis thaliana seedlings reveals changes in metal content

Project description:Plants are exposed to antibiotics produced by soil microorganisms but little is known about their responses at the transcriptional level. Likewise, few endogenous mechanisms of antibiotic resistance have been reported. The Arabidopsis thaliana ATP Binding Cassette (ABC) transporter AtWBC19 (ABCG19) is known to confer kanamycin resistance, but the exact mechanism of resistance is not well understood. Here we examined the transcriptomes of control seedlings and wbc19 mutant seedlings using RNA-seq analysis. Exposure to kanamycin indicated changes in the organization of the photosynthetic apparatus, metabolic fluxes and metal uptake. Elemental analysis showed a 60% and 80% reduction of iron uptake in control and wbc19 mutant seedlings respectively, upon exposure to kanamycin. The drop in iron content was accompanied by the upregulation of the gene encoding for FERRIC REDUCTION OXIDASE 6 (FRO6) in mutant seedlings but not by the differential expression of other transport genes known to be induced by iron deficiency. In addition, wbc19 mutants displayed a distinct expression profile in the absence of kanamycin. Most notably, the expression of several zinc ion binding proteins, including ZINC TRANSPORTER 1 PRECURSOR (ZIP1), was increased, suggesting abnormal zinc uptake. Elemental analysis confirmed a 50% decrease of zinc content in wbc19 mutants. Thus, the antibiotic resistance gene WBC19 appears to also have a role in zinc uptake. Examination of transcriptome in control and wbc19 mutant seedlings with or without exposure to kanamycin.

2014-06-20 | E-GEOD-58662 | biostudies-arrayexpress

An early endosomal network participates to enterocyte functions and intestinal homeostasis

Project description:Membrane trafficking is defined as the vesicular transport of molecules throughout the cell. In intestinal enterocytes, defects in endocytic/recycling pathways impair their function and are linked to genetic diseases. How does trafficking regulate intestinal tissue homeostasis is poorly understood. Using the Drosophila intestine as an in vivo model system, we investigated enterocyte-specific functions for early endosomal trafficking in gut homeostasis. We focused on the small GTPase Rab21 that regulates specific early endosomal trafficking steps. Rab21-depleted guts showed severe intestinal morphology abnormalities, with deregulated homeostasis associated with a gain in mitotic cells and increased cell death. Increased in both apoptosis and Yki signaling were responsible for compensatory proliferation and tissue inflammation. Using a RNAi screen, we identified autophagy and specific membrane trafficking regulators phenocopying Rab21 loss. We further showed that Rab21-induced hyperplasia was rescued by inhibition of Egfr signaling, and we identified improperly trafficked cargoes in enterocytes depleted of Rab21. Our data shed light on an important role for the early endosomal protein Rab21, and early endosomal trafficking in enterocytes-mediated intestinal homeostasis.

2022-08-12 | PXD022413 | Pride

RNA-seq analysis of the effect of kanamycin and the ABC transporter AtWBC19 on Arabidopsis thaliana seedlings reveals changes in metal content

2014-06-20 | GSE58662 | GEO

METAL RUST

Project description:METAL RUST Metagenome

| PRJNA347281 | ENA