Prrc2a, Proline rich coiled-coil 2A, is an m6A reader that plays crucial roles in multiple biological processes. It is involved in regulating mRNA metabolism and translation, and is associated with pathways related to cell differentiation, development, and disease [1,2,3]. Genetic models, especially gene knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions.

Germ cell-specific knockout of Prrc2a in mice leads to XY asynapsis, impaired meiotic sex chromosome inactivation, and meiotic arrest at metaphase I during spermatogenesis, indicating its essential role in male fertility [1]. Nestin-Cre-mediated knockout in mice shows that Prrc2a controls oligodendrocyte specification and myelination, as its deletion causes hypomyelination, decreased lifespan, and locomotive and cognitive defects [2]. In the context of cancer, intestinal epithelium-specific deletion of Prrc2a suppresses tumor cell growth, stemness, and migratory capacity in colorectal cancer, while its overexpression promotes these behaviors [3].

In conclusion, Prrc2a is essential for meiosis I completion in spermatogenesis, oligodendroglial specification and myelination, and has a significant impact on cancer progression. KO/CKO mouse models have been key in revealing its role in these biological processes and disease conditions, providing valuable insights into potential therapeutic targets for male infertility, hypomyelination-related neurological diseases, and cancers such as colorectal cancer [1,2,3].