| First Author | Vanderluit JL | Year | 2007 |
| Journal | J Cell Biol | Volume | 178 |
| Issue | 1 | Pages | 129-39 |
| PubMed ID | 17591923 | Mgi Jnum | J:134919 |
| Mgi Id | MGI:3790045 | Doi | 10.1083/jcb.200703176 |
| Citation | Vanderluit JL, et al. (2007) The Retinoblastoma family member p107 regulates the rate of progenitor commitment to a neuronal fate. J Cell Biol 178(1):129-39 |
| abstractText | The Retinoblastoma protein p107 regulates the neural precursor pool in both the developing and adult brain. As p107-deficient mice exhibit enhanced levels of Hes1, we questioned whether p107 regulates neural precursor self-renewal through the repression of Hes1. p107 represses transcription at the Hes1 promoter. Despite an expanded neural precursor population, p107-null mice exhibit a striking reduction in the number of cortical neurons. Hes1 deficiency rescues neurosphere numbers in p107-null embryos. We find that the loss of a single Hes1 allele in vivo restores the number of neural precursor cells at the ventricular zone. Neuronal birthdating analysis reveals a dramatic reduction in the rate of neurogenesis, demonstrating impairment in p107(-/-) progenitors to commit to a neuronal fate. The loss of a single Hes1 allele restores the number of newly generated neurons in p107-deficient brains. Together, we identify a novel function for p107 in promoting neural progenitor commitment to a neuronal fate. |
