Prmt9, also known as FBXO11, is a protein arginine N-methyltransferase. It is involved in multiple biological processes, including regulation of RNA translation, DNA damage response, innate antiviral immune response, RNA alternative splicing, and cell survival pathways. Its activities are associated with maintaining normal cellular functions and are implicated in various disease conditions [1,2,3]. Genetic models, such as knockout and conditional knockout mouse models, have been crucial in studying its functions.

In a Prmt9 conditional knockout (cKO) mouse model, knockout of Prmt9 in hippocampal neurons led to alternative splicing of about 1900 genes, resulting in aberrant synapse development and impaired learning and memory. This shows that Prmt9 is important for normal neuronal development through its role in regulating RNA splicing [3]. In acute myeloid leukemia (AML), ablation of Prmt9 in AML cells decreased the arginine methylation of regulators of RNA translation and DNA damage response, suppressing cell survival. Additionally, PRMT9 inhibition promoted DNA damage and activated cyclic GMP-AMP synthase, underlying the type I IFN response, suggesting its potential as an anticancer target [1].

In conclusion, Prmt9 is essential for normal neuronal development and plays a role in cell survival and immune evasion in cancer cells. The Prmt9 cKO mouse model has significantly contributed to understanding its role in neuronal development, and studies in AML cells highlight its potential as a target for cancer treatment.