Fhdc1, also known as INF1, is a non-FDD-type Formin homology protein with FH1 and FH2 domains in the N-terminal part and FDCH1-FDCH5 domains in the C-terminal part [2]. It is crucial for coordinating the dynamics of actin and microtubule networks, which is essential for many cellular processes such as cell division, migration, Golgi ribbon formation, and cilia assembly [1,3,4].

Knocking down FHDC1 inhibits actin wave formation in mast cells, indicating its role as an early regulator in formin-mediated actin polymerization [1]. In mammalian cells, knockdown of FHDC1 expression results in defective Golgi assembly, suggesting its importance in maintaining the Golgi-derived microtubule network [3]. Overexpression of FHDC1 affects ciliogenesis, with most cells showing blocked cilia assembly while the present cilia are elongated, and FHDC1 depletion inhibits cilia assembly and induces cilia resorption [4].

In conclusion, Fhdc1 is vital for coordinating cytoskeletal dynamics in multiple cellular processes. The findings from knockdown experiments, which can be considered as a form of loss-of-function study similar to gene knockout in principle, have revealed its significance in actin-microtubule crosstalk, Golgi morphology regulation, and cilia length control. This understanding of Fhdc1's functions may provide insights into related cellular malfunctions and potential disease mechanisms [1,3,4].