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RNA structure and heterologous recombination in the double-stranded RNA bacteriophage phi 6

S Onodera1, X Qiao, P Gottlieb

  • 1Department of Microbiology, Public Health Research Institute, New York, New York 10016.

Journal of Virology
|August 1, 1993
PubMed

Insights

Genetic instability in bacteriophage phi 6 is caused by complementary homopolymer tracts. Removing these tracts or truncating genomic segments stabilizes insertions and facilitates recombinational rescue.

Area of Science:

  • Molecular biology
  • Virology
  • Genetics

Background:

  • Bacteriophage phi 6 possesses a three-segmented double-stranded RNA genome (L, M, S).
  • Genetic insertions into the M segment can exhibit instability due to high recombination rates.
  • Complementary homopolymer tracts flanking inserted genes are implicated in this instability.

Purpose of the Study:

  • To investigate the mechanisms underlying genetic instability in bacteriophage phi 6.
  • To determine the role of homopolymer tracts in recombination rates.
  • To identify conditions that promote or stabilize genetic insertions.

Main Methods:

  • Insertion of kanamycin resistance (kan) and lacZ' genes into the M segment of bacteriophage phi 6.
  • Manipulation of flanking homopolymer tracts to assess their effect on genetic stability.
  • Analysis of phage replication and recombination rates under various conditions.

Main Results:

  • Insertion of the kan gene was unstable due to flanking homopolymer tracts, but stabilization occurred upon removal of one tract.
  • Insertion of lacZ' genes resulted in stable Lac+ phages, with instability arising from complementary homopolymer arms.
  • Truncation of genomic segments or insertion of large genes leading to replication defects facilitated recombinational rescue.

Conclusions:

  • Complementary homopolymer tracts are key drivers of recombinational instability in bacteriophage phi 6.
  • Genetic engineering strategies can stabilize insertions by modifying these tracts.
  • Recombination serves as a rescue mechanism for replication-deficient or damaged viral genomic segments.

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