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Related Experiment Videos

Altered junctional permeability between cells transformed by v-ras, v-mos, or v-src.

M M Atkinson1, J D Sheridan

  • 1Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis 55455.

The American Journal of Physiology
|November 1, 1988
PubMed
Summary

Cancer cell transformation significantly reduces junctional permeability in normal rat kidney (NRK) cells. This rapid change suggests oncogenes like src, ras, and mos impact cell junctions, potentially via protein phosphorylation.

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Area of Science:

  • Cell Biology
  • Oncology
  • Biophysics

Background:

  • Junctional permeability is crucial for normal cell function and communication.
  • Cell transformation by oncogenic viruses alters cellular properties, including intercellular communication.

Purpose of the Study:

  • To quantitatively assess junctional permeability in normal and transformed NRK cells.
  • To investigate the relationship between temperature-sensitive transformation and junctional permeance.
  • To explore the role of specific oncogenes (src, ras, mos) in modulating junctional permeability.

Main Methods:

  • Microinjection of fluorescent dye into NRK cell pairs.
  • Digitization of fluorescence intensity changes using video analysis.
  • Application of Fick's diffusion equation to estimate junctional permeance.

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Main Results:

  • The microinjection and video analysis method reliably estimates junctional permeance.
  • Transformation by Rous sarcoma virus or Moloney murine sarcoma virus reduced junctional permeance by 80-90%.
  • Wild-type Kirsten sarcoma virus also significantly lowered junctional permeance compared to controls.
  • The transformed junctional phenotype was observable as early as 15 minutes post-shift to permissive conditions.

Conclusions:

  • Oncogenic transformation drastically reduces junctional permeability in NRK cells.
  • Oncogenes src, ras, and mos appear to converge on pathways affecting cell junctions.
  • Phosphorylation of junctional proteins is a potential mechanism mediating these effects.