Fmn2, a member of the formin family, is crucial for various cellular processes. It plays a significant role in brain morphogenesis by regulating growth cone motility, which is essential for axonal outgrowth and accurate synaptic targeting. It also participates in axonal collateral branching, a key process in the development of functional neural circuits [1,2].

In growth cone motility, Fmn2 functions as a clutch molecule, mediating the coupling of the actin cytoskeleton to the growth substrate via point contact adhesion complexes, thereby generating traction stresses necessary for growth cone translocation [1]. In axonal collateral branching, Fmn2 localizes to axonal F-actin patches, regulating their lifetime and size, and protecting them from disassembly by the actin-depolymerizing factor ADF, which is important for the initiation of axonal protrusions that form collateral branches [2].

In conclusion, Fmn2 is a key regulator in neuronal development, especially in growth cone motility and axonal branching. Its malfunction may be associated with neurodevelopmental and neurodegenerative disorders, as well as other diseases such as premature ovarian insufficiency, small cell lung cancer, and colorectal cancer [1,2,3,4,5]. Studies on Fmn2 contribute to a better understanding of the underlying mechanisms of these diseases and may offer potential therapeutic targets.