Acute Deletion of METTL14 in β-cells of adult mice results in glucose intolerance

<b>Introduction</b>: To understand the molecular mechanism of glucose intolerance, we performed RNA sequencing to detect the gene expression in beta-cell <i>Mettl14</i> special knockout mice and wild type mice.<b> Material and Methods</b>: Polyadenylated RNA was further enriched from total RNA by using Dyabeads mRNA Purification Kit. All samples were sequenced using Illumina Hiseq 4000 at the University of Chicago Genomic Facility. Sequence reads were aligned to mouse transcriptome (GRCm38.vM17 downloaded from genecode) and quantified using Kallisto at pair-end mode with 30 tomes bootstrap. Transcript level differential expression analysis was performed using sleuth. Inference of differential expression between WT and beta KO mice was made by likelihood ratio and log fold change was obtained using the Wald test. The inference leveraged bootstrap to take uncertainty of quantification into account and leveraged biological replicates to take account the biological variability.<b> Result: </b>The expression levels of 106 transcripts were significantly altered in beta KO islets compared to WT islets. Among those altered genes, 104 genes were upregulated and 2 genes were downregulated.<b>Conclusion:</b><i> Mettl14</i> special knockout in beta-cell induces glucose intolerance by changing genes trascription.<br>