This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Holland, G D
Right arrow Articles by Risser, R
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Holland, G D
Right arrow Articles by Risser, R

 Previous Article  |  Next Article 

J Virol. 1990 May; 64(5): 2226-2235

Conservation of function of Drosophila melanogaster abl and murine v-abl proteins in transformation of mammalian cells.

G D Holland, M J Henkemeyer, D A Kaehler, F M Hoffmann and R Risser

McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.

ABSTRACT

The Drosophila melanogaster abl and the murine v-abl genes encode tyrosine protein kinases (TPKs) whose amino acid sequences are highly conserved. To assess functional conservation between the two gene products, we constructed Drosophila abl/v-abl-chimeric Abelson murine leukemia viruses. In these chimeric Abelson murine leukemia viruses, the TPK and carboxy-terminal regions of v-abl were replaced with the corresponding regions of D. melanogaster abl. The chimeric Abelson murine leukemia viruses were able to mediate morphological and oncogenic transformation of NIH 3T3 cells and were able to abrogate the interleukin-3 dependence of a lymphoid cell line. We also found that a virus that contained both TPK and carboxy-terminal Drosophila abl regions had no in vitro transforming activity for primary bone marrow cells and lacked the ability to induce tumors in susceptible mice. A virus that replaced only a portion of the v-abl TPK region with that of Drosophila abl had low activity in in vitro bone marrow transformation and tumorigenesis assays. These results indicate that the transforming functions of abl TPKs are only partially conserved through evolution. These results also imply that the TPK region of v-abl is a major determinant of its efficient lymphoid cell-transforming activity.


J Virol. 1990 May; 64(5): 2226-2235




This article has been cited by other articles:

  • Comer, A. R., Ahern-Djamali, S. M., Juang, J.-L., Jackson, P. D., Hoffmann, F. M. (1998). Phosphorylation of Enabled by the Drosophila Abelson Tyrosine Kinase Regulates the In Vivo Function and Protein-Protein Interactions of Enabled. Mol. Cell. Biol. 18: 152-160 [Abstract] [Full Text]  
  • Bennett, R. L., Hoffmann, F. M. (1992). Increased levels of the Drosophila Abelson tyrosine kinase in nerves and muscles: subcellular localization and mutant phenotypes imply a role in cell-cell interactions. Development 116: 953-966 [Abstract]