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Separation of simian virus 40 large-T-antigen-transforming and origin-binding functions from the ability to block

V Cherington1, M Brown, E Paucha

  • 1Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111.

Molecular and Cellular Biology
|March 1, 1988
PubMed

Insights

Simian virus 40 large T antigen effectively inhibits adipocyte differentiation in cells. This inhibition occurs regardless of the antigen's DNA binding or transformation capabilities, highlighting its potent role.

Area of Science:

  • Molecular biology
  • Cell biology
  • Virology

Background:

  • Adipocyte differentiation is a complex process involving specific gene expression.
  • Simian virus 40 (SV40) large T antigen is a viral oncoprotein with known cellular effects.

Purpose of the Study:

  • To investigate the role of wild-type and mutant SV40 large T antigen in blocking adipocyte differentiation.
  • To determine if DNA binding or transformation activity is essential for this inhibitory effect.

Main Methods:

  • Utilized 3T3-F442A cells to model adipocyte differentiation.
  • Assayed differentiation by measuring triglyceride accumulation and glycerophosphate dehydrogenase activity.
  • Quantified mRNA expression for adipocyte-specific markers: glycerophosphate dehydrogenase, adipsin, and adipocyte P2.

Main Results:

  • Wild-type SV40 large T antigen potently blocked adipocyte differentiation.
  • Mutant SV40 large T antigens, defective in DNA binding or transformation, were equally effective in blocking differentiation.
  • Key adipocyte markers (triglyceride accumulation, enzyme activity, and specific mRNAs) were suppressed.

Conclusions:

  • SV40 large T antigen is a potent inhibitor of adipocyte differentiation in 3T3-F442A cells.
  • The inhibition of adipocyte differentiation by SV40 large T antigen does not require its origin-specific DNA binding or transformation functions.

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