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Dietary cysteine enhances intestinal stemness via CD8+ T cell-derived IL-22

ABSTRACT: A critical question in physiology is to understand how tissuesadaptand alter their composition in responsetodietary cues.The mammalian small intestine, avitaldigestive organ thatabsorbs nutrients, is maintainedby rapidly renewing Lgr5+ intestinalstem cells (ISCs) located attheintestinal crypt base. While Lgr5+ ISCs drive intestinal adaptation by altering self-renewing and differentiating divisions inresponse todiverse diets such as high-fat diets and fasting regimens, little is known about howmicronutrients, like amino acids, instruct Lgr5+ ISCfate decisions to control intestinal homeostasis and repair after injury. Here, we demonstrate that cysteine, an essential amino acid, enhances theability of Lgr5+ ISCs to repair intestinal injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE279403 | GEO | 2025/10/22

REPOSITORIES: GEO

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Dietary cysteine enhances intestinal stemness via CD8+ T cell-derived IL-22 [scRNA-seq]

Project description:A critical question in physiology is to understand how tissuesadaptand alter their composition in responsetodietary cues.The mammalian small intestine, avitaldigestive organ thatabsorbs nutrients, is maintainedby rapidly renewing Lgr5+ intestinalstem cells (ISCs) located attheintestinal crypt base. While Lgr5+ ISCs drive intestinal adaptation by altering self-renewing and differentiating divisions inresponse todiverse diets such as high-fat diets and fasting regimens, little is known about howmicronutrients, like amino acids, instruct Lgr5+ ISCfate decisions to control intestinal homeostasis and repair after injury. Here, we demonstrate that cysteine, an essential amino acid, enhances theability of Lgr5+ ISCs to repair intestinal injury.

2025-10-22 | GSE279543 | GEO

RNA-seq of mouse Lgr5+ intestinal stem cells and progenitors following Lkb1 deletion against controls

Project description:Perturbed intestinal epithelial homeostasis demonstrated as decreased Lgr5+ intestinal stem cells (Lgr5 ISCs) and increased secretory lineages were observed in our study where Lkb1 was specfically deleted in Lgr5 ISCs using Lgr5-EGFP-creERT2 (Tamoxifen) deletor. To gain mechanistic insight how Lkb1 maintains intestinal epithelial stem cell homeostasis, Lkb1 deficient ISCs (Lgr5-high cells) and progenitors (Lgr5-low cells) are isolated by flow cytometry and profiled by RNA sequencing to compare with controls (Lkb1 wild type ISCs and progenitors).

2020-02-29 | E-MTAB-6501 | biostudies-arrayexpress

Ribosome impairment regulates intestinal stem cell identity via ZAKa activation.

Project description:The small intestine is a rapidly proliferating organ that is maintained by a small population of Lgr5-expressing intestinal stem cells (ISCs). However, several Lgr5-negative ISC populations have been identified, and this remarkable plasticity allows the intestine to rapidly respond to both the local environment and to damage. The mediators of such plasticity are still largely unknown. Using intestinal organoids and mouse models, we show that upon ribosome impairment (driven by Rptor deletion, amino acid starvation, or low dose cyclohexamide treatment) ISCs gain an Lgr5-negative, fetal-like identity. This is accompanied by a rewiring of metabolism. Our findings suggest that the ribosome can act as a sensor of nutrient availability, allowing ISCs to respond to the local nutrient environment. Mechanistically, we show that this phenotype requires the activation of ZAKɑ, which in turn activates YAP, via SRC. Together, our data reveals a central role for ribosome dynamics in intestinal stem cells, and identify the activation of ZAKɑ as a critical mediator of stem cell identity.

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BMP suppresses Wnt signaling via the Bcl11b-regulated NuRD complex to maintain Lgr5+ intestinal stem cells

Project description:Lgr5+ intestinal stem cells (ISCs) play crucial roles in maintenance of the intestinal epithelium renewal and regeneration after injury. The mechanism underlying the interplay between Wnt and BMP signaling is not fully understood. Here we report that Bcl11b, which is downregulated by BMP signaling, enhances Wnt signaling to maintain Lgr5+ ISCs and promote the regeneration of the intestinal epithelium following damage. Conditional inactivation of the Bcl11b gene leads to a significant decrease of Lgr5+ ISCs in both mouse intestinal crypts and cultured organoids. Mechanistically, BMP suppresses the expression of Bcl11b, which can positively regulate Wnt target genes by inhibiting the function of the Nucleosome Remodeling and Deacetylase (NuRD) complex and facilitating the β-catenin-TCF4 interaction. Bcl11b can also promote intestinal epithelium repair after injuries elicited by both irradiation and DSS-induced inflammation. Furthermore, Bcl11b deletion prevents proliferation and tumorigenesis of colorectal cancer cells. Together, our findings suggest that BMP balances Wnt signaling via Bcl11b to delicately regulate the homeostasis and regeneration of the intestinal epithelium.

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Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [scRNAseq]

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2022-09-08 | GSE185354 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200909Yil]

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Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200211YilA]

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Gene expression profiles of WT and CREPT deleted Lgr5+ intestinal stem cells

Project description:Intestinal stem cells (ISCs) residing in the crypts are critical for the continual self-renewal and rapid recovery of intestinal epithelium. The regulatory mechanism of ISCs is not fully understood. Here we report that CREPT, a recently identified tumor-promoting gene, is preferably expressed in the crypts, where the ISCs reside, but not in the villi. The Lgr5+ ISCs have much higher CREPT protein level than Lgr5- cells. To explore the function of CREPT in ISCs, we isolated WT and CREPT deleted Lgr5+ ISCs (Lgr5-CREPTKO) to perform Next generation sequencing.

2020-11-08 | GSE143604 | GEO

A constant pool of Lgr5+ intestinal stem cells is required for intestinal homeostasis

Project description:Lgr5+ crypt base columnar cells, the operational intestinal stem cells (ISCs), are thought to be dispensable for small intestinal (SI) homeostasis. Using a novel Lgr5-2A-DTR (Diphtheria Toxin Receptor) model which ablates Lgr5+ cells with near-complete efficiency and retains endogenous levels of Lgr5 expression, we show that persistent depletion of Lgr5+ ISCs in fact compromises SI epithelial integrity and reduces epithelial turnover in vivo. In vitro, Lgr5-2A-DTR SI organoids are unable to establish or survive when Lgr5+ ISCs are continuously eliminated when DT is in the media. However, transient exposure to DT at the start of culture allows organoids to form, and the rate of outgrowth reduces with increasing length of DT presence. Our results indicate that intestinal homeostasis requires a constant pool of Lgr5+ ISCs, which is supplied by rapidly reprogrammed non-Lgr5+ crypt populations when pre-existing Lgr5+ ISCs are ablated.

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