Related Experiment Videos

Deletions and insertions within an amino-terminal domain of pp60v-src inactivate transformation and modulate membrane

H C Wang1, J T Parsons

  • 1Department of Microbiology, University of Virginia School of Medicine, Charlottesville 22908.

Journal of Virology
|January 1, 1989
PubMed

Insights

Small deletions in the Rous sarcoma virus src gene (pp60v-src) inactivate cell transformation. Altered src proteins show reduced stability but maintain kinase activity, suggesting a role in membrane association.

Area of Science:

  • Molecular Biology
  • Virology
  • Cell Biology

Background:

  • Previous studies indicated large deletions in the Rous sarcoma virus (RSV) src gene affect cell transformation.
  • The specific domain responsible for transformation and protein stability was not fully elucidated.

Purpose of the Study:

  • To investigate the role of specific amino acid residues within the pp60v-src protein domain (155-175) in chicken cell transformation.
  • To analyze the impact of small deletions and insertions on pp60v-src kinase activity, stability, and membrane association.

Main Methods:

  • Site-directed mutagenesis was used to introduce small deletions and insertions into the pp60v-src gene.
  • Transformation assays were performed using chicken cells.
  • Biochemical analyses assessed protein kinase activity, cellular half-life, and membrane association of mutant src proteins.

Main Results:

  • Small deletions (tri- and tetrapeptide) within residues 155-175 of pp60v-src abolished cell transformation.
  • Insertion of four amino acids at position 161 also inhibited transformation, while a single amino acid insertion did not.
  • Mutant src proteins exhibited only marginal loss of tyrosine kinase activity but had significantly reduced cellular half-lives.
  • These altered src proteins efficiently associated with cellular membranes.

Conclusions:

  • The structural domain encompassing residues 155-177 of pp60v-src is critical for maintaining transformation.
  • This domain may regulate pp60src stability at the cellular membrane, potentially through interactions with membrane components or substrates.
  • Protein stability, rather than kinase activity, appears to be the primary factor affected by mutations in this region.

Related Concept Videos