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Regulation of the junB gene by v-src
1Department of Pediatrics, University of Michigan School of Medicine, Ann Arbor 48109.
Molecular and Cellular Biology
|August 1, 1992
Summary
Viral src (v-src) transformation elevates junB gene expression by altering proteins binding to the junB promoter's TATAA box, independent of ras or raf pathways.
Area of Science:
- Molecular Biology
- Cell Signaling
- Oncogenesis
Background:
- Cellular and viral src proteins transmit mitogenic signals.
- Nuclear targets of these signals remain largely unidentified.
Purpose of the Study:
- Investigate the effect of v-src expression on gene transcription.
- Identify specific regulatory elements and mechanisms involved in src-mediated gene modulation.
Main Methods:
- Utilized transient expression of junB promoter-chloramphenicol acetyltransferase constructs in NIH 3T3 cells.
- Employed deletion and point mutagenesis to map v-src-responsive regions.
- Assessed the role of src tyrosine kinase activity using various src mutants.
Main Results:
- v-src transformation significantly increased junB transcripts, distinct from c-src, v-H-ras, or v-raf.
- A 121-nucleotide region in the junB promoter, including CCAAT and TATAA elements, was identified as v-src-responsive.
- Mutagenesis of the TATAA box abolished v-src responsiveness, indicating modification of TATAA-binding proteins.
- Elevated src tyrosine kinase activity was essential for junB expression changes.
Conclusions:
- Src proteins modulate junB expression via tyrosine kinase activity, targeting the TATAA box region.
- This mechanism appears distinct from ras/raf pathways and may be a common feature in src oncogenic action.
- Suggests src proteins influence nuclear effectors through novel pathways.