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Mutagenesis of the murine cytomegalovirus M56 terminase gene

Jian Ben Wang1, Michael A McVoy1

  • 1Department of Pediatrics, Medical College of Virginia campus of Virginia Commonwealth University, 1101 E. Marshall Street, Richmond, Virginia 23298-0163, USA.

The Journal of General Virology
|October 22, 2008
PubMed

Insights

Murine cytomegalovirus (MCMV) M56 protein is essential for viral replication. Its ATPase active site is critical for MCMV terminase function, DNA packaging, and infectious virus reconstitution.

Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Murine cytomegalovirus (MCMV) M56 protein is a component of the MCMV terminase complex.
  • The terminase complex is essential for viral DNA cleavage and packaging into capsids.
  • Previous studies suggested M56 deletion was lethal to the virus.

Purpose of the Study:

  • To investigate the essentiality of the MCMV M56 protein for viral replication.
  • To determine the role of the putative ATPase active site within M56.
  • To assess the function of the overlapping M56a open reading frame.

Main Methods:

  • Deletion of M56 from a bacterial artificial chromosome (BAC) MCMV genome clone.
  • Reintroduction of M56 and its variants at an ectopic locus.
  • Introduction of mutations targeting the putative ATPase active site and M56a frame shift.

Main Results:

  • M56 deletion from the MCMV BAC clone prevented infectious virus reconstitution.
  • Reintroduction of wild-type M56 restored viral replication to wild-type efficiency.
  • Mutations in the M56 ATPase active site abolished viral viability, while M56a frame shift mutations had no effect.

Conclusions:

  • The MCMV M56 protein is essential for viral replication.
  • Residues in the M56 putative ATPase active site are critical for terminase function.
  • The overlapping M56a open reading frame is dispensable for viral replication.

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