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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [Total RNA-seq - crypts]

ABSTRACT: Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [Total RNA-seq - crypts]

PROVIDER: PRJNA532545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8887370.fastq.gz	Fastqsanger.gz
	SRR8887380.fastq.gz	Fastqsanger.gz
	SRR8887390.fastq.gz	Fastqsanger.gz
	SRR8887371.fastq.gz	Fastqsanger.gz
	SRR8887381.fastq.gz	Fastqsanger.gz

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [Total RNA-seq - crypts]

Project description:Aging is a complex multifactorial process leading to the loss of tissue/organ functionality and to an increase in disease risk. Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Many molecular mechanisms related to dysfunction and diseases are well-known (e.g. in cancer), however how aging impact on them before the occurrence of dysfunctions and diseases is poorly understood. In this study, we applied a multi-layered omics-approach to characterize the transcriptional and the epigenetic landscape of mouse intestinal epithelium during aging. We found gender and cell-type specific transcriptional and epigenetic alterations on key pathways and genes linked to intestinal dysfunctions, stem cell aging, organismal lifespan and cancer. Moreover, we identified a switch in the composition of the old intestinal stem cell subpopulations, represented by a drift towards a more secretory lineage committed (and less stem) state accompanied by functional epigenetic alterations.

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [scRNA-seq].

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases

Project description:Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [scRNA-seq].

Project description:Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases [scRNA-seq].

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases. [Total RNA-seq - Lgr5]

Project description:Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases. [Total RNA-seq - Lgr5]

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Transcriptional and epigenetic landscape of the mouse intestine during aging identifies key molecular drivers of aging -associated dysfunctions and diseases

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression data from DSS-treated crypts, normal colon crypts and tumor crypts

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Project description:Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Influence of aging on intestinal stem cell (ISC) and their niches can explain underlying causes for perturbation in ISC function during aging. However, molecular mechanisms for such decrease in functionality of ISCs during aging remain largely undetermined. Using different transcriptome-wide approaches including single-cell RNA-seq from intestinal crypt cells and immune cells of lamina propria, we characterized age-specific transcriptional programs in the intestinal epithelium. We found that aged ISCs strongly upregulate antigen presenting pathway genes and over-express secretory lineage marker genes leading to a compromised homeostasis of the intestinal epithelium. Mechanistically, increase of interferon gamma (IFNgamma) release by cytotoxic CD4 T cells and innate lymphoid type 2 cells (ILC2) in lamina propria of aged intestine lead to induction of Stat1 in ISCs that trigger MHC class II expression and prime them towards a secretory fate. Altogether these findings, clarify the cross talk between immune cells and ISC in aged intestine and identified the IFNgamma-Stat1-MHCII axis as the key gene network driving intestinal inflammaging phenotype and loss of tissue homeostasis. Our data provide basic and complementary knowledge for the development of therapeutic intervention for aging-related intestinal dysfunction and diseases.

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