Ontology highlight
ABSTRACT:
PROVIDER: PRJNA437010 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6808090_1.fastq.gz | Fastqsanger.gz | |||
| SRR6808090_2.fastq.gz | Fastqsanger.gz | |||
| SRR6808100_1.fastq.gz | Fastqsanger.gz | |||
| SRR6808100_2.fastq.gz | Fastqsanger.gz | |||
| SRR6808091_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:During weaning, the transition from milk to solid food rapidly expands and diversifies the gut microbiome, triggering the weaning reaction, a programmed immune response critical for long-lasting mucosal immunity. We characterized how these microbiome changes from weaning through young adulthood in mice shape the DNA methylome and transcriptome of intestinal stem cells (ISCs). We identified a weaning-induced IFN-g–TET3 axis as a key driver of MHC class II enhancer-linked epigenetic reprogramming, creating a transcriptional memory that persists through differentiation into adulthood. Early-life disruption of this axis, via IFN-g blockade or low-dose penicillin, impaired microbiota-mediated epigenetic control and mucosal immunity. Weaning-associated microbiome shifts enriched metabolites such as α-ketoglutarate, Fe2+, and methionine g-lyase, promoting TET-dependent DNA demethylation. These findings reveal how early-life events imprint lifelong epigenetic regulation of mucosal immunity, highlighting epithelial cells as innate immune sentinels that acquire trained transcriptional memory in response to microbial cues.
2026-02-06 | GSE275219 | GEO
Project description:During weaning, the transition to solid food diversifies the gut microbiome, triggering a programmed immune response critical for long-lasting mucosal immunity. Previous work showed that the gut microbiome mediates epigenetic development in intestinal stem cells (ISCs) during suckling, but what happens during weaning is unclear. Here, using genome-wide methylation profiling revealed that weaning-driven microbiome changes shape the DNA methylome and transcriptome of murine ISCs in an IFN-g dependent manner. Specifically, we observe demethylation of enhancer elements essential for MHC class II genes, which result in a transcriptional memory that persists through differentiation into adulthood. IFN-g blockade, or low-dose penicillin to target Gram-positive bacteria, in early life impaired microbiome-mediated epigenetic control and mucosal immunity, and exacerbated colitis. Murine organoids primed with IFN-g showed rapid, amplified transcriptional responses upon secondary stimulations. These findings reveal that early-life events alter the gut microbiome and these changes reprogram ISC epigenetic memory to shape mucosal immunity.
2026-02-06 | GSE275418 | GEO
Project description:During weaning, the shift from milk to solid food is accompanied by a rapid expansion and diversification of the gut microbiome. This triggers the weaning reaction, a programmed immune response important for long-lasting mucosal immunity that is poorly understood. Here, we characterize the impact of the gut microbiome on the DNA methylome and transcriptome of intestinal stem cells (ISCs) from weaning to young adulthood in mice. We identify a weaning- IFN-g-TET3 axis that reprograms epithelial MHC-II signaling via enhancer demethylation in ISCs, establishing a lasting transcriptional memory into adulthood. Disruption of this axis by IFN-g blockade or low-dose penicillin attenuates the microbiota-mediated epigenetic control of epithelial MHC-II signaling, leading to impaired mucosal immunity. By engaging immune crosstalk and metabolite production, the weaning microbiome drives epigenetic reprogramming, thereby establishing a microbiome-induced regulatory pathway that couples developmental cues to lifelong epithelial immune resilience.
2026-02-06 | GSE310995 | GEO
Project description:Feed additives aiming to improve gastrointestinal health are frequently supplied to piglets after weaning but might be more effective when administered before weaning. In this period, feed additives can either be administered directly to neonates, or indirectly via sow’s feed. It is yet unknown what the effect of the administration route is on gut functionality and health. Therefore, we compared the effect of different dietary interventions on gut functionality after maternal administration (lactation feed) to the neonatal administration route (oral gavage). These feed interventions included medium chain fatty acids (MCFA), beta-glucans (BG), and galacto-oligosaccharides (GOS). We measured intestinal gene expression and microbiota composition after birth (d1) and after weaning (d31). Our results show that the type of intervention and the administration route influence gut functionality (microbiome and gene expression profiles). MCFA administration led to a more differentially orchestrated response when comparing the neonatal and maternal administration route then the other two additives, indicating the route of administration of the feed interventions is determinative for the outcome. This implies that for each nutritional intervention in early life of a pig the optimal route of administration needs to be determined.
2023-06-01 | GSE229947 | GEO
Project description:Infant gut microbiome maturation during weaning
| PRJEB97976 | ENA
Project description:The objective of this experiment was to use transcriptional profiling of skeletal muscle and adipose tissue to develop a better understanding of the metabolic basis for poor weaned-pig transition. A total of 1,054 pigs were reared in commercial conditions and weighed at birth, weaning, and 3 weeks post- weaning. Transition average daily gain (tADG) was calculated as the average daily gain for the 3-week period post-weaning. Nine pigs from each of the lowest 10th percentile (low tADG) and the 60th-70th percentile (high tADG) were harvested at 3 weeks post-weaning. Differential expression analysis was conduced in both tissues using RNA-Seq methodology mRNA profiling in two different tissues (skeletal muscle and adipose tissue) harvested at 3 weeks post-weaning
2015-02-25 | E-GEOD-65983 | biostudies-arrayexpress
Project description:Weaning diet switch brings gut microbiome maturation along with postnatal formation of sufficient matured β-cell mass. The matured gut microbiota elevated agonistic components of bile acid (BA) pool towards farnesoid X receptor (FXR) that was paralleling with the declined β-cell FXR expression. To investigate whether BA/FXR could link postnatal β-cell development and gut microbiota maturation, we forced persistent FXR expression in β cells (βFxrKI) and found decreased neonatal β-cell mass growth and increased glycemia in weaned βFxrKI mice, which could be partially recovered by ablating gut microbiota before weaning. scRNA and scATAC seq analysis showed different β cell growth trajectories with suppressed intrinsic cell proliferation and elevated cell apoptosis in βFxrKI. Caspase-6 was then identified as a dominant β-cell FXR downstream effector to mediate its regulation. The negative regulation of the FXR-Casp6 axis on postnatal β-cell mass expansion reflected a programmed cellular response to gut microbiota maturation in neonatal mice.
2025-11-13 | GSE241406 | GEO
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation. C57BL6 mice were divided into low-dose penicillin or control groups. Given antibiotics via drinking water after weaning. Sacrificed and liver sections collected for RNA extraction.
2012-06-30 | E-GEOD-38880 | biostudies-arrayexpress
Project description:The objective of this experiment was to use transcriptional profiling of skeletal muscle and adipose tissue to develop a better understanding of the metabolic basis for poor weaned-pig transition. A total of 1,054 pigs were reared in commercial conditions and weighed at birth, weaning, and 3 weeks post- weaning. Transition average daily gain (tADG) was calculated as the average daily gain for the 3-week period post-weaning. Nine pigs from each of the lowest 10th percentile (low tADG) and the 60th-70th percentile (high tADG) were harvested at 3 weeks post-weaning. Differential expression analysis was conduced in both tissues using RNA-Seq methodology
2015-02-25 | GSE65983 | GEO