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Enterochromaffin cells act as intestinal signal integration hubs for microbial metabolites

ABSTRACT: Enterochromaffin cells act as intestinal signal integration hubs for microbial metabolites

PROVIDER: PRJNA1208584 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31947231_1.fastq.gz	Fastqsanger.gz
	SRR31947231_2.fastq.gz	Fastqsanger.gz
	SRR31947232_1.fastq.gz	Fastqsanger.gz
	SRR31947232_2.fastq.gz	Fastqsanger.gz
	SRR31947233_1.fastq.gz	Fastqsanger.gz

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Enterochromaffin cells act as intestinal signal integration hubs for microbial metabolites

Project description:The intestinal epithelium senses and responds to the myriad of signals from gut microbiota, but it remains unclear how these signals are integrated to drive physiological responses. In this work, we found that enterochromaffin (EC) cells in the gut serve as signal integration hubs for microbial metabolites. EC cells coordinate responses to combinations of microbial metabolites, resulting in complex alterations in serotonin signaling that drive changes in GI physiology. We found that microbial metabolites either directly trigger responses or alter the expression of receptors for other microbial metabolites in EC cells. The microbiota-derived purine derivative hypoxanthine triggers a signaling pathway by activating G-protein coupled receptor A1R, which in turn activates the calcium channel TRPC4, resulting in increased serotonin release and accelerated GI transit. On the other hand, bacteria-derived butyrate does not evoke EC cell calcium influx by itself, but drives epigenetic changes that upregulate TRPC4 expression, thereby enhancing response to metabolites like hypoxanthine and norepinephrine that act via TRPC4. Since the expression TRPC4 is limited to EC cells, these cells function as specialized epithelial sensors that integrate signals from regulatory (butyrate) and effector metabolites like hypoxanthine and norepinephrine. These findings offer new microbiota-driven therapeutic avenues for conditions associated with altered GI function.

2025-02-10 | GSE286305 | GEO

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CRISPR screens unveil signal hubs for nutrient licensing of T cell immunity [CRISPR screen]

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ecDNA hubs drive cooperative intermolecular oncogene expression [HiChIP]

Project description:Extrachromosomal DNA (ecDNA) is prevalent in human cancers and mediates high oncogene expression through gene amplification and altered gene regulation. Gene induction typically involves cis regulatory elements that contact and activate genes on the same chromosome. Here we show that ecDNA hubs, clusters of ~10-100 ecDNAs within the nucleus, enable intermolecular enhancer-gene interactions to promote oncogene overexpression in trans. ecDNAs encoding multiple distinct oncogenes form hubs in diverse cancer cell types and primary tumors. Each ecDNA is more likely to transcribe the oncogene when spatially clustered with additional ecDNAs. ecDNA hubs are tethered by the BET protein BRD4 in a MYC-amplified colorectal cancer cell line. BET inhibitor JQ1 disperses ecDNA hubs and preferentially inhibits ecDNA-based oncogene transcription. A BRD4-bound promoter in PVT1 is ectopically fused to MYC and duplicated in ecDNA, receiving promiscuous enhancer input to drive potent MYC expression. PVT1 promoter on a heterologous episome suffices to mediate gene activation in trans by ecDNA hubs in a JQ1-sensitive manner. Systematic CRISPRi silencing of ecDNA enhancers reveal intermolecular enhancer-gene activation among multiple oncogene loci amplified on distinct ecDNAs. Together, these results demonstrate that ecDNA hubs are protein-tethered clusters of ecDNAs which enable intermolecular transcriptional regulation. ecDNA hubs may act as units of oncogene function, cooperative evolution, and potential targets for cancer therapy.

2020-11-25 | GSE159985 | GEO

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