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Characterization of the interaction between the restriction endonuclease McrBC from E. coli and its cofactor GTP

U Pieper1, T Brinkmann, T Krüger

  • 1Institut für Biochemie (FB 15), Justus-Liebig-Universität Giessen, Heinrich-Buff-Ring 58, Giessen, D-35392, Germany.

Journal of Molecular Biology
|September 23, 1997
PubMed

Insights

The restriction enzyme McrBC utilizes GTP binding and hydrolysis for DNA cleavage. McrB binds GTP strongly, while McrC enhances GTP hydrolysis, crucial for its enzymatic activity.

Area of Science:

  • Molecular Biology
  • Enzymology
  • Bacterial Genetics

Background:

  • McrBC is a GTP-dependent restriction enzyme in E. coli K-12.
  • It cleaves methylated DNA at specific sites (PumCN40-80PumC).
  • Consensus sequences suggest GTP-binding capability in McrBC subunits.

Purpose of the Study:

  • To investigate the GTP-binding and hydrolysis activities of McrBC subunits.
  • To identify the specific subunit responsible for nucleotide binding and hydrolysis.
  • To characterize the role of McrC in McrBC's enzymatic function.

Main Methods:

  • GTP binding affinity measurements using purified McrB.
  • Thermal denaturation assays to assess protein stability upon GTP binding.
  • GTP hydrolysis rate assays in the presence of Mg2+.
  • Enzyme kinetics studies with and without McrC and substrate DNA.
  • Site-directed mutagenesis to identify key residues in nucleotide binding motifs.

Main Results:

  • McrB exhibits high affinity for GTP (10^6 M-1), stabilizing it against denaturation.
  • GTP binding is significantly stronger than GDP or ATP binding.
  • McrB hydrolyzes GTP at a rate of ~0.5 min-1, enhanced 30-fold by McrC.
  • Substrate DNA does not affect GTPase activity.
  • Mutagenesis identified NTAD as the critical motif for guanine nucleotide binding.

Conclusions:

  • McrB is the subunit responsible for GTP binding and hydrolysis in McrBC.
  • McrC acts as a positive regulator, stimulating the GTPase activity of McrB.
  • The NTAD motif is essential for the guanine nucleotide-binding function of McrBC.

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