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DNA-directed mutations. Leading and lagging strand specificity.

R R Sinden1, V I Hashem, W A Rosche

  • 1Department of Biochemistry and Biophysics, Texas A&M University, Houston 77030-3303, USA. RSINDEN@IBT.TAMU.EDU

Annals of the New York Academy of Sciences
|July 23, 1999
PubMed
Summary

Defined order sequence DNA (dosDNA) can form non-B DNA structures, increasing mutation rates during DNA replication. These structures cause deletions on the lagging strand and strand switches on the leading strand.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA replication fidelity ensures accurate genome duplication but can be disrupted by non-B DNA conformations.
  • Defined order sequence DNA (dosDNA) can adopt alternative structures like hairpins and triplexes, potentially causing mutations.

Purpose of the Study:

  • To investigate the impact of dosDNA elements on spontaneous mutagenesis during DNA replication.
  • To analyze strand-specific mutational events induced by direct and inverted repeats.

Main Methods:

  • Cloning of mutational inserts with direct or inverted repeats into a plasmid system in Escherichia coli.
  • Utilizing a unidirectional origin of replication and a selectable marker to track mutations.
  • Analyzing mutations specific to leading and lagging DNA strands.
Keywords:
NASA Discipline Radiation HealthNon-NASA Center

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Main Results:

  • Deletions between direct repeats, stabilized by DNA secondary structures, occurred predominantly on the lagging strand.
  • Intermolecular strand switch events, converting quasipalindromes to perfect inverted repeats, were favored during leading strand replication.

Conclusions:

  • Non-B DNA conformations arising from dosDNA elements significantly influence DNA replication fidelity.
  • The distinct DNA secondary structures formed by direct and inverted repeats lead to strand-specific mutational outcomes.