In this study, we used zebrafish as an animal model to elucidate the developmental function of cdk10 in vertebrates. In situ
hybridization analyses demonstrated that cdk10 is expressed throughout the development, with a relative enrichment in the
brain in the late stages. Similar to its mammalian ortholog, cdk10 can interact with the transcription factor Ets2 and exhibit
kinase activity by phosphorylating histone H1. Morpholino-based loss of cdk10 expression caused apoptosis in sox2-positive
cells and decreased the expression of subsequent neuronal markers. Acetylated tubulin staining revealed a significant reduction
in the number of Rohon-Beard sensory neurons in cdk10 morphants. This result is similar to that demonstrated by decreased
islet-2 expression in the dorsal regions. Moreover, cdk10 morphants exhibited a marked loss of huC-positive neurons in the
telencephalon and throughout the spinal cord axis. The population of retinal ganglion cells was also diminished in cdk10 morphants.
These phenotypes were rescued by co-injection of cdk10 mRNA. Interestingly, the knockdown of cdk10 significantly elevated
raf1a mRNA expression. Meanwhile, the MEK inhibitor (U0126) recovered sox2 and ngn1 transcript levels in cdk10 morphants.
Our findings provide the first functional characterization of cdk10 in vertebrate development and reveal its critical function
in neurogenesis by modulation of raf1a expression.