The Identification of a Glucuronyltransferase-Related Gene, with Putative Mucus Protection and Anti-Inflammatory Effects from Gut-Damaged by Dextran Sulfate Sodium (DSS).

The intestinal epithelium, which is protected by mucosal surfaces composed of mucins and other glycoproteins, functions as a selective barrier that absorbs nutrients while preventing the translocation of harmful substances. To understand the mechanisms between mucosal disruption and tissue inflammation, we orally administrated a mucus-disrupting agent, dextran sodium sulfate, to and screened 63 differentially expressed genes (DEGs). Through a database search using bioinformatics tools (CHEA3 and WebGestalt), we identified ELK1 as a potential key transcription factor for the selected DEGs, and among the 63 DEGs, ELK1-related genes, B3GAT3, FIBP, and TENT2 (, , and in ), were selected as the relevant genes that respond to mucus disruption. We confirmed that enterocyte (EC)-specific knockdown by RNAi significantly reduced gut length and increased intestinal stem cell proliferation in . Additionally, in EC-specific -knockdown flies, it was observed that the mucus-production-related genes, and , were specifically reduced, whereas the inflammatory cytokines and were overexpressed. This study provides evidence that is involved in the regulation of intestinal inflammation in and plays a protective role against mucus disruption. Our findings suggest that may be a potential therapeutic target for the treatment of intestinal inflammatory diseases such as IBD.