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Spatial transcriptomic studies of the small intestine from WT and DDX5△IEC (KO) mice

ABSTRACT: Spatial transcriptomic studies of the small intestine from WT and DDX5△IEC (KO) mice

PROVIDER: PRJNA765044 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15999537_1.fastq.gz	Fastqsanger.gz
	SRR15999537_2.fastq.gz	Fastqsanger.gz
	SRR15999538_1.fastq.gz	Fastqsanger.gz
	SRR15999538_2.fastq.gz	Fastqsanger.gz

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Spatial transcriptomic studies of the small intestine from WT and DDX5△IEC (KO) mice

Project description:DDX5, a DEAD box containing RNA binding protein, is involved in multiple aspects of RNA metabolism and is abundantly expressed in all subsets of the intestinal epithelial cells (IEC). Here, we characterized the DDX5-dependent transcriptome in the small intestine. In the DDX5△IEC tissue, we found that secretory IEC lineage progenitor containing spots (Atoh1hi and Sox4hi) had reduced expression of Pou2f3, a master regulator of a subset of IECs called tuft cells. As a result of the loss of Pou2f3 expression in the progenitors, DDX5△IEC tissue harbored lower number of tuft cell containing spots (Dclk1hi) compare to WT tissues.

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Expression data from colon samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic colitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

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Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic ileitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

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Project description:Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid-binding protein 1 (FABP1). However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that an RNA binding protein DDX5 augments C3 and FABP1 expressions post-transcriptionally to promote tumorigenesis in the colon and small intestine, respectively. Mice with epithelial-specific knockout of DDX5 are protected from intestine tumorigenesis. The identification of DDX5 as the common upstream regulator of tissue-specific oncogenic molecules provides a new therapeutic target for intestine cancers.

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