Stern, Claudio D. and Norris, Wendie E. and Carlson, Geoffrey J. and Faissner, Andreas and Keynes, Roger J. and Schachner, Metlitta and Bronner, Marianne E. (1989) J1/tenascin-related molecules are not responsible for the segmented pattern of neural crest cells or motor axons in the chick embryo. Development, 107 (2). pp. 309-319. ISSN 0950-1991 http://resolver.caltech.edu/CaltechAUTHORS:STEdev89
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It has been suggested that substrate adhesion molecules of the tenascin family may be responsible for the segmented outgrowth of motor axons and neural crest cells during formation of the peripheral nervous system. We have used two monoclonal antibodies (M1B4 and 578) and an antiserum [KAF9(1)] to study the expression of J1/tenascin-related molecules within the somites of the chick embryo. Neural crest cells were identified with monoclonal antibodies HNK-1 and 20B4. Young somites are surrounded by J1/tenascin immunoreactive material, while old sclerotomes are immunoreactive predominantly in their rostral halves, as described by other authors (Tan et al. 1987--Proc. natn. Acad. Sci. U.S.A. 84, 7977; Mackie et al. 1988--Development 102, 237). At intermediate stages of development, however, immunoreactivity is found mainly in the caudal half of each sclerotome. After ablation of the neural crest, the pattern of immunoreactivity is no longer localised to the rostral halves of the older, neural-crest-free sclerotomes. SDS-polyacrylamide gel electrophoresis of affinity-purified somite tissue, extracted using M1B4 antibody, shows a characteristic set of bands, including one of about 230 x 10(3), as described for cytotactin, J1-200/220 and the monomeric form of tenascin. Affinity-purified somite material obtained from neural-crest-ablated somites reveals some of the bands seen in older control embryos, but the high molecular weight components (120-230 x 10(3] are missing. Young epithelial somites also lack the higher molecular mass components. The neural crest may therefore participate in the expression of J1/tenascin-related molecules in the chick embryo. These results suggest that these molecules are not directly responsible for the segmented outgrowth of precursors of the peripheral nervous system.
|Additional Information:||Copyright © 1989 by Company of Biologists. (Accepted 26 June 1989) This work was supported by a grant from Action Research for the Crippled Child to CDS. MBF, who is a Sloan Foundation Research Fellow, is supported by grants from USPHS (HD-15527), March of Dimes (1-896), and the Muscular Dystrophy Association. AF and MS are supported by the German Research Society. MS is a member of the Swiss Federal Institute of Technology, Zurich.|
|Subject Keywords:||tenascin, cytotactin, J1, segmentation, somites, neural crest, motor axons, peripheral nervous system, substrate-adhesion molecules (SAMs)|
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|Deposited On:||09 Sep 2008 20:27|
|Last Modified:||26 Dec 2012 10:17|
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