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Conformation of NADP+ bound to a type II dihydrofolate reductase

R M Brito1, F B Rudolph, P R Rosevear

  • 1Department of Biochemistry, Rice University, Houston, Texas 77005.

Biochemistry
|February 12, 1991
PubMed

Insights

Type II dihydrofolate reductases (DHFRs) confer trimethoprim resistance. Researchers characterized RBG200, an R388 DHFR derivative, and determined the NADP+ binding conformation using transferred NOEs.

Area of Science:

  • Biochemistry
  • Enzymology
  • Molecular Biology

Background:

  • Type II dihydrofolate reductases (DHFRs) from R67 and R388 plasmids confer trimethoprim resistance.
  • These plasmid-derived DHFRs differ structurally and sequentially from chromosomal DHFRs.

Purpose of the Study:

  • To characterize the physical properties of RBG200, a derivative of R388 DHFR.
  • To determine the conformation of NADP+ bound to RBG200 DHFR.

Main Methods:

  • Cloning and characterization of RBG200.
  • Analysis of RBG200.NADP+ binary complexes using transferred Nuclear Overhauser Effect (NOE) spectroscopy.
  • Distance geometry calculations to model NADP+ conformation.

Main Results:

  • RBG200 transfers the pro-R hydrogen of NADPH to dihydrofolate, classifying it as A-stereospecific.
  • Two distinct RBG200.NADP+ binary complexes were identified, with slow interconversion.
  • Weak binding affinity of NADP+ to RBG200 (KD = 1.9 +/- 0.4 mM).
  • Transferred NOEs revealed syn conformation at the nicotinamide-ribose bond and anti conformation at the adenine-ribose bond of bound NADP+.

Conclusions:

  • The study elucidates the structural basis of NADP+ binding to a plasmid-derived DHFR.
  • Understanding these interactions is crucial for developing new antimicrobial strategies targeting DHFR enzymes.

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