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The CML-specific P210 bcr/abl protein, unlike v-abl, does not transform NIH/3T3 fibroblasts
Science (New York, N.Y.)
|July 31, 1987
Summary
The P210 bcr/abl protein, implicated in chronic myelogenous leukemia (CML), does not transform fibroblasts alone. Viral gag sequences are necessary for bcr/abl to induce fibroblast transformation, suggesting a role in membrane localization.
Area of Science:
- Oncogenesis
- Molecular Biology
- Cellular Transformation
Background:
- The v-abl oncogene efficiently transforms fibroblasts and causes leukemia.
- The role of the related bcr/abl gene product in human chronic myelogenous leukemia (CML) is unclear.
Purpose of the Study:
- To investigate the transforming potential of the P210 bcr/abl protein, the CML-specific gene product.
- To determine the requirements for bcr/abl-mediated fibroblast transformation.
Main Methods:
- Expression of complementary DNA clones encoding the P210 bcr/abl protein in NIH/3T3 fibroblasts.
- Isolation and characterization of transforming bcr/abl recombinants.
Main Results:
- The P210 bcr/abl protein did not transform NIH/3T3 fibroblasts, unlike the v-abl oncogene product (P160).
- Cell lines expressing high levels of P210 bcr/abl remained morphologically normal.
- A transforming bcr/abl recombinant was identified, incorporating viral gag sequences at the NH2-terminus.
Conclusions:
- The P210 bcr/abl protein alone lacks the ability to transform fibroblasts.
- Viral gag sequences, potentially through myristylation-dependent membrane localization, are essential for bcr/abl-mediated fibroblast transformation.