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Analysis of a temperature-sensitive mutation affecting the integration protein of Moloney murine leukemia virus

P L Schwartzberg1, M J Roth, N Tanese

  • 1Department of Biochemistry, Columbia University College of Physicians and Surgeons, New York, New York 10032.

Virology
|February 1, 1993
PubMed

Insights

A Moloney murine leukemia virus mutation causes temperature-sensitive replication and integrase (IN) protein function. This finding reveals a critical role for the pol gene

Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Previous research identified mutations in the Moloney murine leukemia virus pol gene affecting provirus integration.
  • Most prior mutations were lethal to viral replication.

Purpose of the Study:

  • To investigate the impact of a specific pol gene mutation (in6161-12) on Moloney murine leukemia virus replication and integrase function.
  • To characterize the temperature-sensitive phenotype associated with this mutation.

Main Methods:

  • Site-directed mutagenesis to create a 12-base pair linker insertion (in6161-12) at the 3' end of the pol gene.
  • Assessing viral replication and integrase (IN) protein function at different temperatures.

Main Results:

  • The in6161-12 mutation confers a temperature-sensitive phenotype to the virus.
  • Both viral replication and integrase (IN) protein function are impaired at the restrictive temperature.

Conclusions:

  • The 3' end of the pol gene is crucial for Moloney murine leukemia virus replication and integrase function.
  • The in6161-12 mutation provides a valuable tool for studying temperature-sensitive aspects of viral replication and IN protein activity.

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