A branching model of lineage differentiation underpinning the neurogenic potential of enteric glia (Bulk gene expression analysis of  small intestinal glia cells in BAC-treated mice.)
Glial cells have been proposed as an endogenous source of progenitors for the treatment of neural deficits. However, the cellular and molecular mechanisms underpinning the neurogenic potential of certain populations of adult glial cells, are not known. Previous studies have indicated that chemical injury of the gut by benzalkonium chloride (BAC) of the gut can activate neuronal markers. To examine whether gut injury can induce in EGCs neurogenic programs similar to those expressed by early ENS progenitors in vivo, we performed bulk RNA-seq of enteric glia isolated from mouse guts 48 hours after BAC treatment. We isolated tdT+ cells (=EGCs) and tdT- cells (=non-glia cells) from the TM of control and BAC-treated Sox10CreERT2;Rosa26tdTomato mice and subjected the samples to bulk RNAseq analysis. Overall design: Tamoxifen-treated Sox10CreERT2;Rosa26tdTomato mice, which express the fluorescent reporter tdTomato (tdT) specifically in the intrinsic glia cell network of the gut, were treated with BAC. At 48 hours post treatment, we isolated enteric glia cells (EGCs, tdT+) and non-glia cells (tdT-) using FACS from four individual mice for each treatment condition (4x EGC Control = Chem_GliaCtrl, 4x non-glia Control = Chem_NonGliaCtrl, 4x EGC BAC = Chem_GliaBAC, 4x non-glia BAC = Chem_NonGliaBAC)