A New Model of Spontaneous Colitis in Mice Induced by Deletion of an RNA m⁶A Methyltransferase Component METTL14 in T Cells.

ABSTRACT:

Background and aims

Mouse models of colitis have been used to study the pathogenesis of inflammatory bowel disease (IBD) and for pre-clinical development of therapeutic agents. Various epigenetic pathways have been shown to play important regulatory roles in IBD. Reversible N⁶-methyladenosine (m⁶A) methylation represents a new layer of post-transcriptional gene regulation that affects a variety of biological processes. We aim to study how deletion of a critical component of m⁶A writer complex, METTL14, in T cells affects the development of colitis.

Methods

Conditional Mettl14 was lineage specifically deleted with CD4-regulated Cre in T cells. Colitis phenotype was determined by H&E staining, colon weight-to-length ratio and cytokine expressio

SUBMITTER: Lu TX 

PROVIDER: S-EPMC7498954 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature