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Published May 16, 2006 | public
Journal Article Open

Development of NG2 neural progenitor cells requires Olig gene function

Abstract

In the adult central nervous system, two distinct populations of glial cells expressing the chondroitin sulfate proteoglycan NG2 have been described: bipolar progenitor cells and more differentiated "synantocytes." These cells have diverse neurological functions, including critical roles in synaptic transmission, repair, and regeneration. Despite their potential importance, the genetic factors that regulate NG2 cell development are poorly understood, and the relationship of synantocytes to the oligodendroglial lineage, in particular, remains controversial. Here, we show that > 90% of embryonic and adult NG2 cells express Olig2, a basic helix-loop-helix transcription factor required for oligodendrocyte lineage specification. Analysis of mice lacking Olig function demonstrates a failure of NG2 cell development at embryonic and perinatal stages that can be rescued by addition of a transgene containing the human OLIG2 locus. These findings show a general requirement for Olig function in NG2 cell development and highlight further roles for Olig transcription factors in neural progenitor cells.

Additional Information

© 2006 by The National Academy of Sciences of the USA. Edited by Gerald D. Fischbach, Columbia University College of Physicians and Surgeons, New York, NY, and approved April 10, 2006 (received for review December 20, 2005). Published online before print May 8, 2006, 10.1073/pnas.0511001103. This paper was submitted directly (Track II) to the PNAS office. We thank D. Yuk and S. Kaing (both of the Dana-Farber Cancer Institute, Boston) for expert technical assistance and W. Stallcup (Burnham Institute, La Jolla, CA) for kindly providing NG2 antibodies. This work was supported by National Institutes of Health Grants K08NS047213 (to K.L.L.) and R01NS40511 (to D.H.R.). D.J.A. is a Howard Hughes Medical Investigator, and D.H.R. is a Harry Weaver Scholar of the National Multiple Sclerosis Society.

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August 22, 2023
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