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The cellular src gene product regulates junctional cell-to-cell communication
R Azarnia1, S Reddy, T E Kmiecik
1Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33136.
Science (New York, N.Y.)
|January 22, 1988
Summary
Overexpression of the cellular src gene reduces cell communication. This protein tyrosine kinase activity, linked to pp60c-src, impacts gap junctional communication, crucial for development and growth.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Cell-to-cell communication is vital for multicellular organisms.
- Gap junctions mediate direct intercellular communication.
- The cellular src gene product, pp60c-src, is a protein tyrosine kinase implicated in cell regulation.
Purpose of the Study:
- To investigate the role of cellular src gene overexpression in regulating gap junctional communication.
- To determine the correlation between pp60c-src activity and communication.
- To explore the impact of specific mutations on src-mediated communication.
Main Methods:
- NIH 3T3 cells were used to study gene overexpression.
- Point mutations were introduced at Tyr527 and Tyr416.
- Cell-to-cell transmission of molecules (400-700 daltons) was measured.
- Protein tyrosine kinase activity of pp60c-src was assessed.
Main Results:
- Overexpression of the cellular src gene reduced gap junctional communication.
- This down-regulation correlated with pp60c-src kinase activity.
- Mutation of Tyr527 enhanced down-regulation, while mutation of Tyr416 suppressed it.
- Viral-src substitution also enhanced communication down-regulation.
Conclusions:
- Src kinase activity negatively regulates gap junctional communication.
- Specific phosphorylation sites (Tyr527 and Tyr416) are critical for this regulation.
- Src-mediated control of communication may play a role in embryonic development and cellular growth.