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Published December 21, 2006 | Supplemental Material
Journal Article Open

The Transcription Factor NFIA Controls the Onset of Gliogenesis in the Developing Spinal Cord

Abstract

The mechanisms controlling the transition from neurogenesis to gliogenesis in the vertebrate CNS are incompletely understood. We identified a family of transcription factors, called NFI genes, which are induced throughout the spinal cord ventricular zone (VZ) concomitantly with the induction of GLAST, an early marker of gliogenesis. NFIA is both necessary and sufficient for GLAST induction in the VZ. Unexpectedly, NFIA is also essential for the continued inhibition of neurogenesis in VZ progenitors. This function is mediated by the requirement of NFIA for the expression of HES5, a Notch effector. However, Notch effectors are unable to promote glial-fate specification in the absence of NFIA. Thus, NFIA links the abrogation of neurogenesis to a generic program of gliogenesis, in both astrocyte and oligodendrocyte VZ progenitors. At later stages, NFIA promotes migration and differentiation of astrocyte precursors, a function that is antagonized in oligodendrocyte precursors by Olig2.

Additional Information

© 2006 Elsevier B.V. Under an Elsevier user license. Received: May 8, 2006; revised: September 12, 2006; accepted: November 16, 2006; published: December 20, 2006. We thank Stephanie Adams and Rochelle Diamond for assistance with the FACS experiments; and Elizabeth Zhou (Stanford) for assistance in performing the microarray hybridization. The analysis of the microarray data was aided by the Millard and Muriel Jacobs Genetics and Genomics Laboratory at California Institute of Technology. We thank Shirley Pease, Bruce Kennedy, and the staff of the Transgenic Animal Facility at California Institute of Technology (Caltech) for assistance with mouse breeding and care. We thank Bruce Hay for providing the p35 plasmid. Monica Martinez for assistance in cloning the various RCAS-shRNAi, RCAS-NFI constructs and mouse genotyping; J.-S. Chang for technical assistance; G. Mosconi for laboratory management; G. Mancuso for administrative assistance; Yosuke Mukouyama and Tim Lebestky for helpful discussion and critical comments on the manuscript. This work was supported by funding from the Howard Hughes Medical Institute, the Pritzker Neurogenesis Consortium, and the National Institutes of Health 1R01-NS23476 (D.J.A.) and 1F32NS048666 (B.D.). D.J.A. is an investigator of the Howard Hughes Medical Institute.

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