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The physiological roles of aryl hydrocarbon receptor (AhR) in the small intestine have been revealed as immunomodulatory and barrier functions. However, its contributions to cell fate regulation are incompletely understood. The Notch-activated signaling cascade is a central component of intestinal cell fate determinations. The lateral inhibitory mechanism governed by Notch directs cell fates toward distinct cell lineages (i.e., absorptive and secretory cell lineages) through its downstream effector, mouse atonal homolog 1 (MATH1). An investigation employing cell lines and intestinal crypt cells revealed that AhR regulates  Math1  expression in a xenobiotic response element (XRE)-dependent manner. The AhR- Math1  axis was further addressed using intestinal organoids, where AhR- Math1  and HES1- Math1  axes appeared to coexist within the underlying  Math1  transcriptional machinery. When the HES1- Math1  axis was pharmacologically suppressed, β-naphthoflavone-mediated AhR activation increased the number of goblet and Math1 +  progenitor cells in the organoids. The same pharmacological dissection of the AhR- Math1  axis was applied in vivo, demonstrating an enhanced number of Math1 +  progenitor cells in the small intestine following AhR activation. We report here that AhR- Math1  is a direct transcriptional axis with effects on Math1 +  progenitor cells in the small intestine, highlighting a novel molecular basis for fine-tuning Notch-mediated cell fate regulation.

Transcriptional Regulation of Math1 by Aryl Hydrocarbon Receptor: Effect on Math1 + Progenitor Cells in Mouse Small Intestine