Cdc14b, a member of the dual-specificity phosphatases (DUSPs) family, was originally thought to be involved in mitotic exit like its yeast counterpart, but subsequent studies suggest functional specialization in higher eukaryotes. It is now recognized as a key regulator of gene expression and has roles in neuronal development. It may also be involved in meiosis and other developmental processes [1].

In knockout studies, Cdc14b knockout mouse embryonic fibroblasts (MEFs) showed defects in repairing ionizing radiation-induced DNA double-strand breaks (DSBs), especially when Cdc14A levels were low, indicating redundancy between Cdc14B and Cdc14A in DSB repair. Cdc14B deficiency impaired both homologous recombination (HR) and nonhomologous end joining (NHEJ) [4]. In human RPE1 cells, single-and double-knockouts of Cdc14A and Cdc14B did not affect mitotic phases, cytokinesis, or cell proliferation, but cycling Cdc14B KO cells had more frequent and faster-disassembling cilia [3]. In mouse oocytes, overexpression of Cdc14B significantly delayed meiotic resumption, while depletion of Cdc14B led to spontaneous meiotic resumption, suggesting it is a negative regulator of meiotic resumption [2].

In conclusion, Cdc14b has diverse functions in DNA repair, ciliogenesis, and meiotic regulation. The gene knockout models in mice and human cell lines have revealed its role in these biological processes. Understanding Cdc14b is crucial for further exploring normal biological functions and related disease mechanisms, such as potential implications in DNA damage-related diseases and neuronal development disorders.