We have used in situ hybridization and reverse transcriptase polymeras
e chain reaction (PCR) to study the origins of the extracellular matri
x glycoprotein tenascin during the development of the central and peri
pheral nervous systems. Previous studies have shown that neural crest
cells migrate along pathways that are lined with tenascin. In situ hyb
ridization, PCR, and western blotting reveal that these cells themselv
es are a major source of tenascin both in vitro and in the embryo. Thu
s, tenascin is probably not acting as a guidance molecule but is more
likely to be promoting neural crest cell motility in a more general wa
y. Similarly, subpopulations of proliferating and migrating glia make
tenascin in the developing central nervous system, as do the radial gl
ia that are used as a substratum for migrating neuronal cell bodies to
be expressed in the cerebellum by Golgi epithelial cells. This expres
sion, as well as the expression of tenascin in connective tissue, indi
cates that this molecule may also be playing a role in regulating diff
erentiation. Finally, the distribution of tenascin transcripts in the
developing brain and spinal cord is similar to the distribution of mRN
As encoding receptors for platelet-derived growth factor-AA and basic
fibroblast growth factor. In vitro studies indicate that both of these
factors are potential regulators of tenascin expression.