Binding and melting of D-loops by the Bloom syndrome helicase. Academic Article uri icon

Overview

abstract

  • Bloom syndrome is a rare autosomal disorder characterized by predisposition to cancer and genomic instability. BLM, the structural gene mutated in individuals with the disorder, encodes a DNA helicase belonging to the RecQ family of helicases. These helicases have been established to serve roles in both promoting and preventing recombination. Mounting evidence has implicated a function for BLM during DNA replication; specifically, BLM might be involved in rescuing stalled or collapsed replication forks by a recombination-based mechanism. We have tested this idea by examining the binding and melting activity of BLM on oligonucleotide substrates containing D-loops, DNA structures that model the presumed initial intermediate formed during homologous recombination. We find that BLM preferentially melts those D-loops that are formed more favorably by the strand exchange protein Rad51, but whose polarity could be less favorable for enabling restoration of an active replication fork. We propose a model in which BLM selectively dissociates recombination intermediates likely to be unfavorable for recombination-promoted replication.

publication date

  • November 28, 2000

Research

keywords

  • Adenosine Triphosphatases
  • Bloom Syndrome
  • DNA Damage
  • DNA Helicases
  • DNA-Binding Proteins
  • Nucleic Acid Conformation

Identity

Scopus Document Identifier

  • 0034727684

Digital Object Identifier (DOI)

  • 10.1021/bi0018640

PubMed ID

  • 11087418

Additional Document Info

volume

  • 39

issue

  • 47