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The Lambda Select cII Mutation Detection System

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Is FapyG mutagenic?: Evidence from the DFT study.

Nihar Ranjan Jena¹, Phool Chand Mishra

¹Discipline of Natural Sciences, Indian Institute of Information Technology, Design and Manufacturing, Khamaria, Jabalpur-482005 (India); Current address School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane QLD 4072 (Australia). nrjena@iiitdmj.ac.in.

Chemphyschem : a European Journal of Chemical Physics and Physical Chemistry

|August 13, 2013

Summary

2,6-diamino-4-oxo-5-formamidopyrimidine (FapyG), an oxidized guanine product, is non-mutagenic in bacteria but causes G to T mutations in mammals. This study explains FapyG

Keywords:

DNA damage cancer density functional calculations muagenesis nucleobases

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Area of Science:

Biochemistry
Molecular Biology
Computational Chemistry

Background:

2,6-diamino-4-oxo-5-formamidopyrimidine (FapyG) is a major oxidative guanine (G) lesion.
FapyG is considered non-mutagenic in bacteria but mutagenic in mammalian cells, causing G to T mutations.

Purpose of the Study:

To elucidate the molecular mechanisms underlying FapyG's differential mutagenicity in bacterial versus mammalian cells.
To investigate the base-pairing properties of FapyG with DNA bases (C, A, T) in different conformations.

Main Methods:

Density Functional Theory (DFT) calculations were employed to study FapyG base-pair interactions.
Analysis of binding energies and base-pair alignments for FapyG with C, A, and T in anti- and syn-conformations.
Evaluation of solvation effects on FapyG's coding properties.

Main Results:

The anti-FapyG:C base pair exhibits the highest binding energy, mimicking normal G:C pairing, explaining its non-mutagenic behavior in bacteria.
Mammalian polymerases may misinterpret FapyG as thymine (T) due to similar binding patterns of FapyG:A and T:A base pairs.
This mispairing leads to the insertion of adenine (A) opposite FapyG, causing G to T transversions.

Conclusions:

FapyG's non-mutagenic role in bacteria is attributed to preferential C insertion opposite anti-FapyG.
Differential polymerase recognition in mammalian cells leads to FapyG-mediated G to T mutations.
Understanding FapyG coding properties is crucial for explaining oxidative DNA damage-induced mutagenesis.