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A stress-responsive miRNA regulates BMP signaling to maintain tissue homeostasis

ABSTRACT: A stress-responsive miRNA regulates BMP signaling to maintain tissue homeostasis

PROVIDER: PRJNA718188 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14092132.fastq.gz	Fastqsanger.gz
	SRR14092133.fastq.gz	Fastqsanger.gz
	SRR14092134.fastq.gz	Fastqsanger.gz
	SRR14092135.fastq.gz	Fastqsanger.gz
	SRR14092136.fastq.gz	Fastqsanger.gz

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A stress-responsive miRNA regulates BMP signaling to maintain tissue homeostasis

Project description:Adult organisms must sense, respond, and adapt to environmental fluctuations. In high-turnover tissues such as the intestine, these adaptive responses require rapid changes in gene expression that, in turn, likely involve post-transcriptional gene control. However, intestinal tissue specific microRNA mediated regulatory pathways remain unexplored. Here we report the role of an intestinal specific microRNA, miR-958, that non-cell autonomously regulates stem cell numbers during tissue homeostasis and regeneration in the Drosophila adult midgut. We identify its downstream target cabut, the Drosophila ortholog of mammalian KLF10/11 transcription factors, which mediates this miR-958 function by promoting paracrine enterocyte-to-stem cell BMP signaling. We also show that mature miR-958 levels transiently decrease in response to stress, and that this decrease is required for proper stem cell expansion during tissue regeneration. In summary, we have identified a novel post-transcriptional mechanism that modulates BMP signaling activity within Drosophila adult intestinal tissue both during normal homeostasis as well as tissue regeneration to regulate intestinal stem cell numbers.

2021-05-01 | GSE171030 | GEO

A stress-responsive miRNA regulates BMP signaling to maintain tissue homeostasis.

Project description:Adult organisms must sense and adapt to environmental fluctuations. In high-turnover tissues such as the intestine, these adaptive responses require rapid changes in gene expression that, in turn, likely involve posttranscriptional gene control. However, intestinal-tissue-specific microRNA (miRNA)-mediated regulatory pathways remain unexplored. Here, we report the role of an intestinal-specific miRNA, miR-958, that non-cell autonomously regulates stem cell numbers during tissue homeostasis and regeneration in the Drosophila adult midgut. We identify its downstream target cabut, the Drosophila ortholog of mammalian KLF10/11 transcription factors, which mediates this miR-958 function by promoting paracrine enterocyte-to-stem-cell bone morphogenetic protein (BMP) signaling. We also show that mature miR-958 levels transiently decrease in response to stress and that this decrease is required for proper stem cell expansion during tissue regeneration. In summary, we have identified a posttranscriptional mechanism that modulates BMP signaling activity within Drosophila adult intestinal tissue during both normal homeostasis and tissue regeneration to regulate intestinal stem cell numbers.

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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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