Tent5a, also known as FAM46A, is a cytoplasmic poly(A) polymerase. It is involved in post-transcriptional regulation by polyadenylating specific mRNAs, which affects their stability and translation. This function is crucial for various biological processes, and genetic models like KO mouse models are valuable for studying its roles [2,3,4].

In Tent5a knockout mouse models, it was found that Tent5a is required for proper bone formation. Mutations in Tent5a were identified in congenital bone disease osteogenesis imperfecta patients. The Tent5a KO mouse line shows bone fragility and skeletal hypomineralization due to collagen defects, as Tent5a polyadenylates mRNAs encoding Col1α1, Col1α2, and other osteogenesis-related secreted proteins [2].

In addition, Tent5a knockdown in in vitro C2C12 cells (a myoblast cell line) inhibited cell proliferation and migration, and also inhibited the maturation of type I muscle fibers in vitro and in vivo. Mechanistically, this was associated with decreased myogenin expression [1].

In the context of gametogenesis, Tent5a knockout substantially lowers fertility, though not directly related to gametogenesis. Tent5a is also involved in re-adenylation of SARS-CoV-2 mRNA vaccines in macrophages, enhancing their efficacy [3,5].

In conclusion, Tent5a plays essential roles in bone formation, muscle fiber formation, gametogenesis, and vaccine efficacy through its function as a cytoplasmic poly(A) polymerase. The use of Tent5a KO mouse models has been instrumental in revealing its functions in bone-related diseases such as osteogenesis imperfecta, as well as in other biological processes [1,2,3,5].