| First Author | Wang J | Year | 2024 |
| Journal | Biochem Biophys Res Commun | Volume | 695 |
| Pages | 149421 | PubMed ID | 38171233 |
| Mgi Jnum | J:344221 | Mgi Id | MGI:7573767 |
| Doi | 10.1016/j.bbrc.2023.149421 | Citation | Wang J, et al. (2023) JADE1 is dispensable for the brain development in mice. Biochem Biophys Res Commun 695:149421 |
| abstractText | In mammalian brain development, WNT signaling balances proliferation and differentiation of neural progenitor cells, and is essential for the maintenance of regular brain development. JADE1 is a candidate transcription co-factor essential for DNA replication, cell division, and cell cycle regulation. In 293T cells, JADE1 is stabilized by von Hippel-Lindau protein pVHL, promotes the beta-catenin ubiquitination and thus blunts canonical WNT signaling. Furthermore, JADE1 inhibits beta-catenin-induced ectopic axis formation in Xenopus embryos. However, JADE1's role in mammalian brain development remains unknown. Here, we generated a new Jade1 knockout mouse line using CRISPR-Cas9 technology. We found that JADE1 null resulted in decreased survival rate, reduced body weight and brain weight in mice. However, histological analysis revealed a normal brain development. Furthermore, Jade1 null neural progenitor cells proliferated normally in vivo and in vitro. RNA-seq analysis further showed that JADE1 loss did not affect the cerebral cortex gene expression. Our findings indicate that JADE1 is dispensable for developing the cerebral cortex in mice. |
