RNA m6A methylation promotes IFN-gamma-stimulated intestinal epithelial cell-autonomous anti-Cryptosporidium defense

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Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B702
Abstract ID: 4663

Presenting Author:
Chansorena Pok , Ph.D. Candidate at Rush Univ.

Abstract:

Type II and III interferons (IFNs) are critical to prevent intestinal infection by the parasite Cryptosporidium parvum (C. parvum). RNA modification of N6-methyladeonosine (m6A) aids in RNA stability and translation efficiency which may promote protein expression of immune-related genes for pathogen clearance. We hypothesized that m6A methylation of interferon-responsive mRNA transcripts aids in pathogen clearance, thus C. parvum has developed strategies to suppress host m6A methylation. We found that when intestinal epithelial cells were infected with C. parvum there was an upregulation of selected immunity-related RNA genes companied with a decrease in RNA m6A methylation of those genes. Contrastingly, when treated with IFN-g both m6A methylation and RNA levels of those genes were upregulated. The difference in m6A methylation levels in host cells following C. parvum infection and IFN-g stimulation brings the question if m6A methylation is manipulated by both for their own benefit. Additionally, we present data on how the host long-noncoding RNA acts as a regulator of m6A. Our study suggests an important role for m⁶A RNA modifications in regulating expression of immune genes and intestinal epithelial anti-C. parvum defense.