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Background  In the developing vertebrate nervous system elevated levels of Notch signaling activity can block neurogenesis and promote formation of glial cells. The mechanisms that limit Notch activity to balance formation of neurons and glia from neural precursors are poorly understood.    Results  By screening for mutations that disrupt oligodendrocyte development in zebrafish we found one allele, called  vu56 , that produced excess oligodendrocyte progenitor cells (OPCs). Positional cloning revealed that the  vu56  allele is a mutation of  fbxw7 , which encodes the substrate recognition component of a ubiquitin ligase that targets Notch and other proteins for degradation. To investigate the basis of the mutant phenotype we performed in vivo, time-lapse imaging, which revealed that the increase in OPC number resulted from production of extra OPCs by ventral spinal cord precursors and not from changes in OPC proliferation or death. Notch signaling activity was elevated in spinal cord precursors of  fbxw7  mutant zebrafish and inhibition of Notch signaling suppressed formation of excess OPCs.    Conclusion  Notch signaling promotes glia cell formation from neural precursors in vertebrate embryos. Our data indicate that Fbxw7 helps attenuate Notch signaling during zebrafish neural development thereby limiting the number of OPCs.

Fbxw7 regulates Notch to control specification of neural precursors for oligodendrocyte fate