Plet1, also known as C11orf34, is a gene with diverse functions. It encodes a glycophoshatidylinositol (GPI)-anchored surface protein involved in multiple biological processes such as cell migration, tissue repair, and cell fate determination. It plays a role in pathways related to wound healing, immune response, and placental development, which are crucial for normal physiological function [1,2,3,4]. Genetic models, especially KO/CKO mouse models, have been instrumental in studying its functions.

In a KO mouse model, lack of Plet1 in CD11b+ CD103+ dendritic cells (DCs) led to aberrant migratory behavior and their accumulation in the small intestine, suggesting Plet1 facilitates homeostatic interstitial migration of small intestinal DCs [1]. In another model, Plet1 deficiency impaired tissue repair of dextran sulfate sodium (DSS)-induced damage in colon epithelium and reduced tumor formation in an azoxymethane/DSS model of colitis-associated cancer, indicating IL-17A-induced Plet1 expression contributes to tissue repair and colon tumorigenesis [3].

In conclusion, Plet1 is essential for cell migration in the small intestine and for tissue repair and tumorigenesis in the colon. The use of Plet1 KO mouse models has significantly enhanced our understanding of its role in these disease-related processes, providing insights into potential therapeutic strategies for conditions related to impaired tissue repair and colon cancer [1,3].