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Published December 1998 | public
Journal Article

Essential Roles for the Abl and Arg Tyrosine Kinases in Neurulation

Abstract

The Abl and Arg tyrosine kinases play fundamental roles in the development and function of the central nervous system. Arg is most abundant in adult mouse brain, especially in synapse-rich regions. Arg^(−/−) mice develop normally but exhibit multiple behavioral abnormalities, suggesting that arg^(−/−) brains suffer from defects in neuronal function. Embryos deficient in both Abl and Arg suffer from defects in neurulation and die before 11 days postcoitum (dpc). Although they divide normally, abl^(−/−)arg^(−/−) neuroepithelial cells display gross alterations in their actin cytoskeleton. We find that Abl and Arg colocalize with each other and with actin microfilaments at the apical surface of the developing neuroepithelium. Thus, Abl and Arg play essential roles in neurulation and can regulate the structure of the actin cytoskeleton.

Additional Information

© 1998 Cell Press. Received 23 July 1998, Revised 10 November 1998. We would like to thank S. Boast and S. Goff (Columbia University) for advice and the gift of abl² mice (Tybulewicz et al. 1991) and F. Gertler (Massachussetts Institute of Technology), who first noted a significant portion of Abl in the cytoplasm of mouse tissue sections, for assistance in analyzing images. We would like to thank the members of the Gertler, Miczek, and Baltimore Labs for helpful discussions during the course of this work. We are also grateful for the helpful suggestions of two anonymous reviewers. A. J. K. would like to thank M. C. Brown, F. Gertler, B. Howell, T. Jacks, A. McClatchey, G. Schneider, P. Soriano, and especially C. Lois for helpful discussions. This work was supported by a Fellowship from the Jane Coffin Childs Memorial Fund for Cancer Research (A. J. K.), a Special Fellowship from the Leukemia Society of America (A. J. K.), and United States Public Health Service research grants AA5122 and DA02632 (K. A. M.) and CA51462 (D. B.).

Additional details

Created:
August 19, 2023
Modified:
October 20, 2023