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IntroductionExaiptasia diaphana is a popular model organism for exploring the symbiotic relationship observed between cnidarians and their microsymbionts. While physiological roles of algal photosymbionts (Symbiodinaceae) are well studied, the contributions of bacterial communities are less defined in this system.MethodsWe investigated microbial variation between distinct parts of the body and symbiotic state across four genets held in identical environmental conditions using 16s rRNA gene amplicon sequencing.ResultsWe found differentially abundant taxa between body part and symbiotic state that highlight the roles these bacteria may play in holobiont heterotrophy and nutrient cycling. Beta-diversity analysis revealed distinct communities between symbiotic states consistent with previous studies; however, we did not observe the presence of previously reported core microbiota. We also found community differences across clonal lines, despite years of identical rearing conditions. ConclusionThese findings suggest the Exaiptasia bacterial microbiome is greatly influenced by host genetics and unpredictable environmental influences.

Enteroviral infections are implicated in islet autoimmunity and type 1 diabetes (T1D) pathogenesis. Significant β-cell stress and damage occur with viral infection, leading to cells that are dysfunctional and vulnerable to destruction. Human stem cell-derived β (SC-β) cells are insulin-producing cell clusters that closely resemble native β cells. To better understand the events precipitated by enteroviral infection of β cells, we investigated transcriptional and proteomic changes in SC-β cells challenged with coxsackie B virus (CVB). We confirmed infection by demonstrating that viral protein colocalized with insulin-positive SC-β cells by immunostaining. Transcriptome analysis showed a decrease in insulin gene expression following infection, and combined transcriptional and proteomic analysis revealed activation of innate immune pathways, including type I interferon (IFN), IFN-stimulated genes, nuclear factor-kappa B (NF-κB) and downstream inflammatory cytokines, and major histocompatibility complex (MHC) class I. Finally, insulin release by CVB4-infected SC-β cells was impaired. These transcriptional, proteomic, and functional findings are in agreement with responses in primary human islets infected with CVB ex vivo. Human SC-β cells may serve as a surrogate for primary human islets in virus-induced diabetes models. Because human SC-β cells are more genetically tractable and accessible than primary islets, they may provide a preferred platform for investigating T1D pathogenesis and developing new treatments.