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doi: 10.1242/10.1242/dev.00184
1 Wolfson Institute for Biomedical Research and Department of Biology,
University College London, Gower Street, London WC1E 6BT, UK
2 Institute of Molecular and Cell Biology, 30 Medical Drive, Singapore
117609
3 Department of Molecular Biology and Pharmacology, Washington University School
of Medicine, St. Louis, MO 63110, USA
* Author for correspondence (e-mail: w.richardson{at}ucl.ac.uk)
Accepted 3 October 2002
The postnatal central nervous system (CNS) contains many scattered cells
that express fibroblast growth factor receptor 3 transcripts (Fgfr3).
They first appear in the ventricular zone (VZ) of the embryonic spinal cord in
mid-gestation and then distribute into both grey and white matter —
suggesting that they are glial cells, not neurones. The
Fgfr3+ cells are interspersed with but distinct from
platelet-derived growth factor receptor 
(Pdgfra)-positive
oligodendrocyte progenitors. This fits with the observation that
Fgfr3 expression is preferentially excluded from the pMN domain of
the ventral VZ where Pdgfra+ oligodendrocyte progenitors
— and motoneurones — originate. Many glial fibrillary acidic
protein (Gfap)- positive astrocytes co-express Fgfr3 in vitro and in
vivo. Fgfr3+ cells within and outside the VZ also express
the astroglial marker glutamine synthetase (Glns). We conclude that
(1) Fgfr3 marks astrocytes and their neuroepithelial precursors in
the developing CNS and (2) astrocytes and oligodendrocytes originate in
complementary domains of the VZ. Production of astrocytes from cultured
neuroepithelial cells is hedgehog independent, whereas oligodendrocyte
development requires hedgehog signalling, adding further support to the idea
that astrocytes and oligodendrocytes can develop independently. In addition,
we found that mice with a targeted deletion in the Fgfr3 locus
strongly upregulate Gfap in grey matter (protoplasmic) astrocytes, implying
that signalling through Fgfr3 normally represses Gfap expression in vivo.
Key words: Fgfr3, Targeted deletion, Astrocyte, Reactive gliosis, CNS, Neuroepithelium
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