CHD1L Promotes Neuronal Differentiation in Human Embryonic Stem Cells by Upregulating PAX6.

Chromodomain helicase DNA-binding protein 1-like gene (CHD1L) was initially isolated as a candidate oncogene in hepatocellular carcinoma, and it has been associated with many malignancies. Knockdown of Chd1l in zygote-stage mouse embryos resulted in developmental arrest, suggesting that Chd1l is required for mouse early development. However, the exact role of CHD1L in development, especially in humans, has not been reported. In this study, we found that overexpression of CHD1L in human embryonic cells (hESCs) upregulated the expression of ectoderm genes, especially PAX6. Furthermore, ectopic expression of CHD1L promoted hESCs to differentiate into neuroepithelium both in embryoid bodies and in directed neuronal differentiation. Knockdown of CHD1L significantly impaired neuroepithelial differentiation of hESCs. Interestingly, Chd1l colocalized with a PAX6-positive cell population and was highly expressed in the ventricular (germinal) zone of fetal mice. Taken together, these data suggest that CHD1L promotes neuronal differentiation of hESCs and may play an important role in nervous system development.

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