Dysfunctional b-cell autophagy induces b-cell stress and enhances islet immunogenicity
We knocked out the critical autophagy enzyme, ATG7, in the ß-cells of mice (ATG7?ß-cell) then monitored blood glucose to assess the phenotype induced by this KO model. We found that all ATG7?ß-cell mice developed diabetes between 11-15 weeks of age. We isolated islets from ATG7?ß-cell and littermate control mice several weeks prior to diabetes development (7-10 weeks of age) and performed bulk islet mRNA sequencing. The purpose of this experiment was  to understand the islet biological process pathways altered by dysfunctional ß-cell autophagy in the ATG7?ß-cell model. Overall design: RNA-seq profiling of ATG7?ß-cell and littermate control islets several weeks prior to diabetes development.