ANP32B-deficiency suppresses ocular development by repression of PAX6

We observed that the deletion of Anp32b led to severe defects in ocular development, such as anophthalmia and microphthalmia. Moreover, Anp32b was highly expressed in the lens, and Anp32b−/− embryos with microphthalmia typically exhibited severely impaired lens development. Mechanistically, ANP32B directly interacted with paired box protein 6 (PAX6), a master transcriptional regulator of ocular development, and enhanced its transcriptional activity. In line with these findings, overexpression of PAX6 partially but significantly reversed the inhibition of proliferation observed in ANP32B knockdown cells. Collectively, our findings reveal that ANP32B-deficiency suppresses ocular development by repression of PAX6 and identify ANP32B as a viable therapeutic target for ocular developmental defects. RNA-seq data from the eye tissue of Anp32b+/+/ Anp32b−/− embryos