The ups and downs of Pax6 in neural stem cells

Abstract

Neural stem cells (NSCs) must rapidly adapt their transcriptional activity to the ever-changing embryonic environment. Currently, we have a limited understanding of how key transcription factors such as Pax6 are modulated at the protein level. In a recent issue of the JBC, Dong et al identifed a novel post-translational regulatory mechanism in which Kat2a-mediated lysine acetylation on Pax6 leads to its ubiquitination and ultimately its degradation via the proteasome pathway, thereby determining whether NSCs undergo proliferation or neuronal differentiation.