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Replication process of the parvovirus H-1. X. Isolation of a mutant defective in replicative-form DNA replication

Journal of Virology
|January 1, 1978
PubMed

Insights

A new temperature-sensitive mutant, ts14, shows defective parvovirus replicative-form DNA synthesis. This defect is cis-acting and impacts viral DNA replication and protein synthesis, suggesting a regulatory sequence mutation.

Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Parvoviruses are small, single-stranded DNA viruses that replicate in the nucleus of host cells.
  • Replicative-form (RF) DNA synthesis is a critical step in the parvovirus life cycle.
  • Temperature-sensitive mutants are valuable tools for studying viral gene function.

Purpose of the Study:

  • To isolate and characterize a temperature-sensitive mutant of H-1 parvovirus with defects in RF DNA synthesis.
  • To investigate the genetic basis and functional consequences of the observed defect.
  • To explore the interactions of the mutant with other parvoviruses.

Main Methods:

  • Isolation and characterization of a temperature-sensitive mutant (ts14) of H-1 parvovirus.
  • Assay of replicative-form (RF) DNA synthesis at permissive and restrictive temperatures.
  • Complementation analysis using defective H-1 virus (DI-1) and wild-type H-3.
  • Multiplicity-dependent inhibition assays for viral DNA and protein synthesis.
  • Comparative physical mapping of viral DNA.

Main Results:

  • The ts14 mutant exhibited significantly reduced RF DNA synthesis (3-7% of wild-type) at the restrictive temperature.
  • Complementation analysis indicated that the RF DNA synthesis defect is cis-acting.
  • ts14 demonstrated multiplicity-dependent inhibition of DI-1 and H-3 RF DNA synthesis, but not LuIII.
  • Cross-interference was observed in viral protein synthesis, with ts14 inhibiting H-1 and H-3 infectious virus production.
  • Physical mapping suggested higher homology between H-1 and H-3 than between H-1 and LuIII.

Conclusions:

  • The ts14 mutant possesses a defect in a regulatory DNA sequence essential for H-1 parvovirus RF DNA replication.
  • This mutation affects not only viral DNA synthesis but also viral protein synthesis and infectious virus production.
  • The findings provide insights into the regulatory mechanisms governing parvovirus DNA replication and inter-viral interactions.

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