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Two new retroviral onc genes, sea and jun
1Department of Microbiology, University of Southern California, School of Medicine, Los Angeles 90033.
Princess Takamatsu Symposia
|January 1, 1986
Summary
Avian leukemia virus S13 and avian sarcoma virus 17 oncogenes, sea and jun, were studied. The sea oncogene encodes a protein kinase, while jun shows potential DNA-binding activity.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Avian leukemia virus S13 (S13) causes various cancers, including erythroblastosis and fibrosarcoma.
- Avian sarcoma virus 17 (ASV17) is known to induce fibrosarcoma.
- Both viruses transform cells in culture, indicating oncogenic potential.
Purpose of the Study:
- To investigate the oncogenes responsible for the transforming abilities of S13 and ASV17.
- To characterize the molecular mechanisms underlying viral oncogenesis.
Main Methods:
- Analysis of viral oncogenes and their protein products.
- Biochemical assays to determine protein activity.
- Sequence homology analysis.
Main Results:
- S13's oncogene, sea, produces a 155 kDa fusion glycoprotein (gp155) processed into active gp70env-sea with tyrosine-specific protein kinase activity.
- ASV17's oncogene, jun, is expressed as a 55 kDa gag-jun fusion protein.
- The jun protein's C-terminal region shares homology with the DNA-binding domain of yeast GCN4.
Conclusions:
- The sea oncogene product possesses protein kinase activity, contributing to S13-induced neoplasia.
- The jun oncogene product may function as a DNA-binding protein, potentially involved in ASV17-induced fibrosarcoma.
- These findings elucidate distinct molecular mechanisms of oncogenesis by different avian retroviruses.