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Published August 1985 | Published
Journal Article Open

Alterations in neural crest migration by a monoclonal antibody that affects cell adhesion

Abstract

The possible role of a 140-kD cell surface complex in neural crest adhesion and migration was examined using a monoclonal antibody JG22, first described by Greve and Gottlieb (1982, J. Cell. Biochem. 18:221-229). The addition of JG22 to neural crest cells in vitro caused a rapid change in morphology of cells plated on either fibronectin or laminin substrates. The cells became round and phase bright, often detaching from the dish or forming aggregates of rounded cells. Other tissues such as somites, notochords, and neural tubes were unaffected by the antibody in vitro even though the JG22 antigen is detectable in embryonic tissue sections on the surface of the myotome, neural tube, and notochord. The effects of the JG22 on neural crest migration in vivo were examined by a new perturbation approach in which both the antibody and the hybridoma cells were microinjected onto neural crest pathways. Hybridoma cells were labeled with a fluorescent cell marker that is nondeleterious and that is preserved after fixation and tissue sectioning. The JG22 antibody and hybridoma cells caused a marked reduction in cranial neural crest migration, a build-up of neural crest cells within the lumen of the neural tube, and some migration along aberrant pathways. Neural crest migration in the trunk was affected to a much lesser extent. In both cranial and trunk regions, a cell free zone of one or more cell diameters was generally observed between neural crest cells and the JG22 hybridoma cells. Two other monoclonal antibodies, 1-B and 1-N, were used as controls. Both 1-B and 1-N bind to bands of the 140-kD complex precipitated by JG22. Neither control antibody affected neural crest adhesion in vitro or neural crest migration in situ. This suggests that the observed alterations in neural crest migration are due to a functional block of the 140-kD complex.

Additional Information

© 1985 Rockefeller University Press. The Authors acknowledge that RUP will make the Article freely available to the public on RUP's website after expiration of the Initial Publication Period, and that RUP intends to submit the Article to PubMed Central in accordance with PubMed Central's requirements, where the Article will be released to the public after expiration of the Initial Publication Period. After the Initial Publication Period, RUP will grant to the public the non- exclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license as described at http://creativecommons.org/licenses/by-nc-sa/3.0/ and http://creativecommons.org/licenses/by-nc-sa/3.0/legalcode. Received for publication 22 March 1985, and in revised form 27 April 1985. I thank Drs. Scott Fraser and James Coulombe for their helpful comments on the manuscript, and Georgia Guillory and Elizabeth Montgomery for their excellent technical assistance. This work was supported by U.S. Public Health Service grant HD-15527-01 and by a Basic Research Grant from the March of Dimes Birth Defects Foundation.

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Created:
August 19, 2023
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October 18, 2023