The intestinal epithelium exhibits a remarkable degree of cellular plasticity that aids in re-establishing intestinal homeostasis following acute or chronic tissue damage. Although cellular plasticity has been described in the mouse intestinal epithelium using reporter mouse models to label distinct epithelial cell types, a deeper understanding of the cellular states and signaling pathways that are required for undergoing this phenomenon has not yet been developed. Furthermore, the regulatory factors that allow rapid cellular changes that facilitate cellular plasticity are incompletely understood. Here we implement novel flow cytometry-based assays that allow the discrimination of intestinal epithelial cells with the capacity for plasticity based on the amount of autophagic vesicles present. Furthermore, we utilize novel mouse models designed for the interrogation of the role of RNA-binding proteins in regulating cellular plasticity. We show that baseline levels of autophagic vesicles positively correlate with cellular plasticity within the intestinal epithelium. Furthermore, we demonstrate that this phenomenon can be observed when sorting within the enteroendocrine and Paneth cell lineages, suggesting that cellular plasticity based on autophagic vesicle content in the intestinal epithelium is lineage agnostic. We further demonstrate that the RNA-binding protein Imp1 regulates Lrg5+ stem cell maintenance and genetic ablation of Imp1 in intestinal epithelial cells decreases stem cell frequency and enhances cellular plasticity within the epithelium. Finally, we show that Imp1 regulates intestinal regeneration following irradiation in an autophagy-dependent manner. Taken together, this dissertation sheds light on the autophagy pathway as an important determinant of cellular plasticity in the epithelium. Furthermore, we uncover the RNA-binding protein Imp1 as novel regulator of intestinal stem cell state and as potential therapeutic targets for enhancing injury resolution in the intestine.