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Dietary induced epigenetic reprogram in mouse intestinal enterocytes

ABSTRACT: Dietary induced epigenetic reprogram in mouse intestinal enterocytes

PROVIDER: PRJNA947654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23942312_1.fastq.gz	Fastqsanger.gz
	SRR23942312_2.fastq.gz	Fastqsanger.gz
	SRR23942313_1.fastq.gz	Fastqsanger.gz
	SRR23942313_2.fastq.gz	Fastqsanger.gz
	SRR23942314_1.fastq.gz	Fastqsanger.gz

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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

Translatome profiling of Drosophila intestinal enterocytes upon Dietary Restriction

Project description:We determined the actively translated mRNA induced/repressed by a Dietary Restriction intervention specifically in the differentiated enterocytes of the intestine. For this, we did a "genetic dissection" by expressing a tagged ribosomal subunit (RpL13A-His6FLAG) under the control of the tissue specific Myo1A-GAL4 driver, targetting its expression exclusively to the intestinal enterocytes. By performing a anti-flag pulldown we are then able to enrich our mRNA pool for transcripts that are directly bound to ribosomes and being actively translated. In this manner, we become one step closer to protein synthesis while profiling gene expression.

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Project description:Bl6 mice were fed with New Western diet 1 (NWD1) or Americal Instititue of Nutrition 76A (AIN76A or AIN) diet from weaning for 3 months. Single intestinal epithelial cells were FACS isolated by the Epcam+, CD45- , and subject to scACTAseq assay.

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Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [intestinal organoids]

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Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

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Project description:Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [Organoid]

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [In_vivo]

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Influence of development and dietary phospholipid content and composition on intestinal transcriptome of Atlantic salmon (Salmo salar)

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