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PROVIDER: PRJEB75656 | ENA |
REPOSITORIES: ENA
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Project description:Metagenomics of intestinal microbiomes from mice fed different sources of dietary protein
| PRJEB67356 | ENA
Project description:To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions. scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq (available in PRJNA1090629) were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.
2025-02-08 | GSE262229 | GEO
Project description:To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions. scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.
2025-02-08 | GSE262228 | GEO
Project description:intestinal microbiota of fish Metagenome
| PRJNA493193 | ENA
Project description:Although much research has been done on the diversity of gut microbiome, little is known about the way it influences intestinal homeostasis under normal and pathogenic conditions. Epigenetic mechanisms have recently been suggested as operating at the interface between the microbiota and the intestinal epithelium cells (IECs). Using genome-wide analyses, we discovered that exposure to microbiota induced both global DNA hypomethylation and localized changes at regulatory elements, which culminates in activation of a set of “early sentinel” response genes that play a role in maintaining gut homeostasis. Furthermore, we demonstrated that exposure to microbiota in acute inflammation results in profound DNA methylation and chromatin accessibility changes at regulatory elements leading to alterations in the gene expression program in colitis and colon cancer. Our studies add a new dimension to our understanding of the cross talk between the microbiota and IECs, and provide the foundation for how microbiota impact epigenetic programming.
2020-02-06 | GSE141458 | GEO
Project description:Intestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players for tolerance towards microbiota-derived and food-borne antigens, and compelling evidence suggests that intestinal microbiota modulate their differentiation and maintenance. Selected bacterial species and microbiota-derived metabolites such as short-chain fatty acids (SCFAs) have been reported to foster Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites of de novo Treg induction, and we could previously show that mLN stromal cells contribute to this process. Yet, it is not fully elucidated which direct role microbiota and their metabolites play for the early stages of de novo Treg induction and in shaping the Treg transcriptome already during the initial priming within mLNs. Here, we show that neither dysbiotic microbiota nor dietary SCFA supplementation impact de novo induction of Foxp3+ Tregs within mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent frequencies of de novo induced Foxp3+ Tregs within mLNs. Further dissection of the accessible chromatin and transcriptome revealed that microbiota indeed have a limited impact on fostering the establishment of peripherally induced Tregs and do not contribute to the initialization of the epigenetic landscape for an extensive Treg signature. Viewed as a whole, our data suggest that microbiota are dispensable for the early stages of de novo Treg induction within mLNs, while being required to foster further Treg differentiation and homeostasis at later stages within the intestinal lamina propria.
2021-03-24 | GSE150566 | GEO