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A mutant v-rel with increased ability to transform B lymphocytes

P Romero1, E H Humphries

  • 1Mary Babb Randolph Cancer Center, West Virginia University, Morgantown 26506-9162.

Journal of Virology
|January 1, 1995
PubMed
Summary
This summary is machine-generated.

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A specific mutation in v-Rel enhances REV-T

Area of Science:

  • Molecular Biology
  • Virology
  • Oncology

Background:

  • Two strains of REV-T (Reticuloendotheliosis virus strain T) exhibit differential bursal cell transformation capabilities.
  • REV-TW, a wild-type strain, fails to induce bursal cell colonies, while REV-S2A3 readily transforms them.

Purpose of the Study:

  • To investigate the molecular basis for the differential transforming activity of REV-T strains.
  • To identify specific mutations in the v-rel oncogene responsible for enhanced bursal cell transformation.

Main Methods:

  • Polymerase Chain Reaction (PCR) was used to clone and amplify the v-rel gene from REV-S2A3.
  • Site-directed mutagenesis and gene exchange experiments were performed to assess the functional impact of identified mutations.
  • In vitro transformation assays using bursal cells and splenocytes were conducted.

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Main Results:

  • A G-to-T transversion mutation at position 40 of v-rel, changing alanine to serine, was identified in the highly transforming REV-S2A3 strain.
  • Mutant viruses with the alanine-to-serine substitution at position 40 of v-Rel demonstrated enhanced ability to form bursal cell colonies in vitro.
  • Wild-type viruses induced non-B-cell colonies, whereas mutant viruses predominantly generated B-cell colonies.

Conclusions:

  • The substitution of serine for alanine at position 40 of v-Rel significantly enhances the transforming potential of REV-T for B lymphocytes.
  • This mutation, located near the DNA-binding region, increases kappa B-binding activity, correlating with enhanced transformation.
  • The findings highlight the critical role of specific v-Rel mutations in B-cell lymphomagenesis.