Rbm14-KO Mouse

Rbm14, an RNA-binding protein, is involved in multiple essential biological functions. It plays roles in DNA repair pathways such as homologous recombination repair and canonical nonhomologous end-joining. It is also associated with cell cycle regulation, oocyte meiotic maturation, and embryonic development. Additionally, it has been implicated in various disease-related processes like cancer development and virus-host interactions [2,5-10].

In knockout studies, Rbm14 knockout in mice leads to apoptosis and cell proliferation defects in early post-implantation epiblast cells, resulting in gastrulation disruption and embryonic lethality. This indicates its crucial role in maintaining genome integrity during early mouse embryogenesis through mediating alternative splicing of DNA damage response-related genes [1]. In mouse embryonic stem cells, depletion of Rbm14 alters gene expression profiles, downregulating pluripotency-associated genes and those in the Wnt and TGF-β signaling pathways, and it is essential for mesoderm development [2]. In zebrafish and mouse, depletion of Rbm14 impairs embryonic cell differentiations and full activations of the zygotic genome, causing developmental arrest at the blastula stage [3].

In conclusion, Rbm14 is vital for maintaining genome integrity, pluripotency, and early embryonic development. Its knockout models have revealed its significance in these processes. In the context of diseases, Rbm14 has been linked to cancer and virus-related conditions, highlighting its potential as a therapeutic target in these areas.