Abstract
The jun oncoprotein, which causes sarcomas in chickens, and the DNA-binding domain of yeast GCN4, which coordinately regulates the expression of amino acid biosynthetic genes, show significant homology. In yeast cells deleted for the GCN4 gene, GCN4 function can be conferred by a hybrid protein in which the GCN4 DNA-binding domain is replaced by the homologous region of jun. Moreover, in strains containing various mutations of the GCN4 binding site in the HIS3 promoter, HIS3 expression is affected similarly by the hybrid protein and by GCN4. These results indicate that the jun oncoprotein binds the same DNA sequences as GCN4, and strongly suggest that jun is derived from a normal cellular transcription factor (possibly AP-1, which recognizes similar sequences). This provides direct evidence for the idea that alterations in the machinery for proper gene expression can lead to the oncogenic state.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
