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Loss of YAP/TAZ impaired the proliferation and differentiation ability of neural progenitor cells

YAP (Yes-associated protein) and TAZ (transcriptional coactivator with PDZ-binding motif) are downstream effectors of the Hippo pathway, they activate the expression of transcriptional targets that promote cell growth, cell proliferation, and prevent apoptosis. Here we examined the function of YAP/TAZ in mouse neocortex development through conditional deletion of Yap and Taz by Emx1-Cre. Loss of YAP/TAZ cause the hydrocephalus after birth, leads to aberrant development and dilated ventricle in adult stage, this phenotype can be detected as early as P0. YAP/TAZ are expressed in Sox2+ neural progenitor cells, when YAP/TAZ are deleted, the neuroepithelial cell junctions are disrupted; the numbers of Sox2+ cell and Tbr2+ cell are reduced and the ratio of tbr2/Sox2 is also reduced at E17.5. Results of cell cycle analyzing experiments display YAP/TAZ deletion increased the cell cycle exit. The improperly increased expression of Tuj1+ in progenitor cells in the YAP/TAZ deleted cortex indicates the premature of Sox2+ progenitor cells. Together, our results reveal that YAP/TAZ deletion changed the polarity of neuroepithelial cells, and increased the cell cycle exit, reduced the differentiation of Sox2+ cells into Tbr2+ cells through promoting the premature of Tuj1+ cells. These results define the functions of YAP/TAZ in keeping the cell polarity neural progenitors and ensuring their proliferation and differentiation, and also reveal the roles of YAP/TAZ in developing cortex.