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Phenotypic changes induced by wild type and variant c-src genes carrying C-terminal sequence alterations
B A Yatsula1, J Plachy, A Mikhailik
1Unité Mixte de Recherche 146 du Centre National de la Recherche Scientifique, Institut Curie, Orsay, France.
Oncogene
|December 19, 1996
Summary
The oncogenic properties of the c-src gene were investigated. Mutation of tyrosine 527 and C-terminal extension together fully activated c-src
Area of Science:
- Oncology
- Molecular Biology
- Retroviral Research
Background:
- Avian sarcoma retroviruses can transduce proto-oncogenes like c-src.
- The PR2257 retrovirus carries a modified v-src gene with potential oncogenic alterations.
Purpose of the Study:
- To determine the roles of tyrosine 527 mutation and C-terminal extension in c-src oncogenesis.
- To compare the oncogenic potential of wild-type c-src and its variants.
Main Methods:
- Overexpression of wild-type c-src and variants in chicken embryo fibroblasts and neuroretina (NR) cells using retroviruses.
- In vivo assessment of tumorigenicity via plasmid DNA inoculation.
Main Results:
- Overexpression of c-src alone can induce NR cell division.
- Tyrosine 527 mutation significantly activates c-src transforming and tumorigenic properties.
- Combined mutations confer full oncogenic properties and increased metastatic potential.
Conclusions:
- Tyrosine 527 mutation is a key activator of c-src oncogenicity.
- The C-terminal extension enhances oncogenic properties and metastatic potential.
- PR2257's v-src exhibits potent oncogenic activity compared to other strains.