Prrc2a, a Proline rich coiled-coil 2A, functions as an m6A reader. It is involved in crucial biological processes such as spermatogenesis, oligodendrocyte development, and is associated with pathways related to cell cycle regulation, mRNA metabolism, and translation. Its dysregulation is linked to various diseases including hepatocellular carcinoma, colorectal cancer, and autoimmune and neurodegenerative disorders, highlighting its overall biological importance. Genetic models, especially KO/CKO mouse models, are valuable tools for studying Prrc2a's functions [1,2,3,4,5].

Germ cell-specific knockout of Prrc2a in mice causes XY asynapsis, impaired meiotic sex chromosome inactivation, and meiotic arrest at metaphase I during spermatogenesis, revealing its essential role in meiosis I completion [1]. Nestin-Cre-mediated knockout of Prrc2a in mice leads to significant hypomyelination, decreased lifespan, and locomotive and cognitive defects, indicating its role in oligodendrocyte specification and myelination [2]. Intestinal epithelium-specific deletion of Prrc2a in mice suppresses tumor cell growth, stemness, and migratory capacity in colorectal cancer, suggesting its oncogenic role in this disease [4].

In conclusion, Prrc2a, as an m6A reader, plays essential roles in spermatogenesis and oligodendrocyte development. Studies using KO/CKO mouse models have revealed its significance in diseases such as colorectal cancer, and in autoimmune and neurodegenerative disorders, enhancing our understanding of the underlying biological mechanisms and potentially providing new therapeutic targets.