Enterotoxigenic Escherichia coli infection promotes enteric defensin expression via FOXO6-METTL3-m⁶A-GPR161 signalling axis.

ABSTRACT: The production of natural antimicrobial peptides has emerged as an important mechanism of innate immunity in animals. Defensins, members of a large family of antimicrobial peptides, have been suggested as effector molecules in host defence against bacteria, fungi, protozoa and enveloped viruses. However, the molecular mechanism underlying defensin upregulation in bacterial infection remains poorly understood. The modification of mRNA by N6-adenosine methylation (m⁶A) on internal bases influences gene expression in eukaryotes. Here, we show that β-defensin production triggered by Enterotoxigenic Escherichia coli K88 (E. coli K88) infection is controlled by the cellular m⁶A methyltransferase METTL3. Adding back with METTL3 robustly stimulated the re-expres

SUBMITTER: Zong X 

PROVIDER: S-EPMC7971227 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature