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The Heterochromatin protein 1 is a regulator in RNA splicing precision deficient in ulcerative colitis

ABSTRACT: The Heterochromatin protein 1 is a regulator in RNA splicing precision deficient in ulcerative colitis

PROVIDER: PRJNA793233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17383633_1.fastq.gz	Fastqsanger.gz
	SRR17383633_2.fastq.gz	Fastqsanger.gz
	SRR17383634_1.fastq.gz	Fastqsanger.gz
	SRR17383634_2.fastq.gz	Fastqsanger.gz
	SRR17383635_1.fastq.gz	Fastqsanger.gz

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The Heterochromatin protein 1 is a master regulator in RNA splicing precision deficient in ulcerative colitis

Project description:Defects in RNA splicing have been linked to numerous human disorders, but remain poorly explored in inflammatory bowel disease (IBD). Here, we report that, in the gut epithelium of patients with ulcerative colitis (UC), the expression of the chromatin and alternative splicing regulator HP1g is strongly reduced. Accordingly, inactivation of the HP1g gene in the mouse gut triggered several IBD-like traits, including inflammation and dysbiosis. In parallel, we discovered that its loss of function broadly increased splicing noise, reducing requirement for canonical splicing consensus sequences, and favoring the usage of cryptic splice sites at numerous genes with key functions in gut biology. This notably resulted in the production of progerin, a noncanonical toxic splice variant of prelamin A mRNA, responsible for the Hutchinson Gilford Progeria Syndrome (HGPS) of premature aging. Likewise, production of progerin transcript was found to be a signature of colonic cells from UC patients. Thus, our study identifies HP1g as a regulator of RNA metabolism in vivo, providing a unique mechanism linking anti-inflammation and accuracy of RNA splicing in the gut epithelium. HP1 defect may confer a general disturbance in RNA splicing precision to scrutinize in IBD and more generally in accelerating aging diseases.

2022-10-25 | PXD031580 | Pride

The Heterochromatin protein 1 is a regulator in RNA splicing precision deficient in ulcerative colitis.

Project description:Defects in RNA splicing have been linked to human disorders, but remain poorly explored in inflammatory bowel disease (IBD). Here, we report that expression of the chromatin and alternative splicing regulator HP1γ is reduced in ulcerative colitis (UC). Accordingly, HP1γ gene inactivation in the mouse gut epithelium triggers IBD-like traits, including inflammation and dysbiosis. In parallel, we find that its loss of function broadly increases splicing noise, favoring the usage of cryptic splice sites at numerous genes with functions in gut biology. This results in the production of progerin, a toxic splice variant of prelamin A mRNA, responsible for the Hutchinson-Gilford Progeria Syndrome of premature aging. Splicing noise is also extensively detected in UC patients in association with inflammation, with progerin transcripts accumulating in the colon mucosa. We propose that monitoring HP1γ activity and RNA splicing precision can help in the management of IBD and, more generally, of accelerated aging.

| S-EPMC9674647 | biostudies-literature

Ulcerative colitis gene expressions file

Project description:Ulcerative colitis related gene expressions analysis in colonic biopsy samples from control and ulcerative colitis patients

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Project description:The series was designed to identify the different methylated single CpGs involved in the pathophysiology of ulcerative colitis. A cohort of n=20 monozygotic twins, discordant for ulcerative colitis was selected. Illumina and Nimblegen platforms were used.

2012-09-27 | E-GEOD-27899 | biostudies-arrayexpress

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Project description:Through laser capture microdissection and microarray analysis combined with slightly modified RNA extraction and amplification. we could analyze the subtle differential expression between colon normal cell and ulcerative colitis. Keywords: Ulcerative Colitis, amplification, microdissection

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Project description:The samples are a part of a study aiming at diagnosing ulcerative colitis from genome-wide gene expression analysis of the colonic mucosa. Colonic mucosal samples were collected as endoscopic pinch biopsies from ulcerative colitis patients and from control subjects. Samples with and without macroscopic signs of inflammation were collected from the patients. Experiment Overall Design: The series contain eight UC samples with macroscopic signs of inflammation, 13 UC smaples without macroscopic signs of inflammation, five control subjects.

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