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Sequence-specific and Selective Recognition of Double-stranded RNAs over Single-stranded RNAs by Chemically Modified Peptide Nucleic Acids
Published on: September 21, 2017
The L561A substitution in the nascent base-pair binding pocket of RB69 DNA polymerase reduces base discrimination
Hong Zhang1, Chanu Rhee, Anna Bebenek
1Department of Molecular Biophysics and Biochemistry, Yale University, 333 Cedar Street, New Haven, Connecticut 06520, USA.
Abstract:
Several variants of RB69 DNA polymerase (RB69 pol) with single-site replacements in the nascent base-pair binding pocket are less discriminating with respect to noncomplementary dNMP incorporation than the wild-type enzyme. To quantify the loss in base selectivity, we determined the transient-state kinetic parameters for incorporation of correct and all combinations of incorrect dNMPs by the exonuclease-deficient form of one of these RB69 pol variants, L561A, using rapid chemical quench assays. The L561A variant did not significantly alter the k(pol) and K(D) values for incorporation of correct dNMPs, but it showed increased incorporation efficiency (k(pol)/K(D)) for mispaired bases relative to the wild-type enzyme. The incorporation efficiency for mispaired bases by the L561A variant ranged from 1.5 x 10(-)(5) microM(-)(1) s(-)(1) for dCMP opposite templating C to 2 x 10(-)(3) microM(-)(1) s(-)(1) for dAMP opposite templating C. These k(pol)/K(D) values are 3-60-fold greater than those observed with the wild-type enzyme. The effect of the L561A replacement on the mutation frequency in vivo was determined by infecting Escherichia coli harboring a plasmid encoding the L561A variant of RB69 pol with T4 phage bearing a mutant rII locus, and the rates of reversions to rII(+) were scored. The exonuclease-proficient RB69 pol L561A displayed a weak mutator phenotype. In contrast, no progeny phage were produced after infection of E. coli, expressing an exonuclease-deficient RB69 pol L561A, with either mutant or wild-type T4 phage. This dominant-lethal phenotype was attributed to error catastrophe caused by the high rate of mutation expected from combining the pol L561A and exo(-) mutator activities.
Insights
RB69 DNA polymerase variants show reduced base selectivity, increasing mutation rates. The L561A variant exhibits a dominant-lethal phenotype in vivo due to error catastrophe when lacking exonuclease activity.
Area of Science:
- Molecular Biology
- Biochemistry
- Genetics
Background:
- DNA polymerases are crucial for DNA replication and repair, ensuring fidelity through base selection.
- Mutations in DNA polymerases can lead to genomic instability and disease.
- RB69 DNA polymerase (RB69 pol) is a model enzyme for studying polymerase fidelity.
Purpose of the Study:
- To quantify the loss of base selectivity in RB69 pol variants with mutations in the nascent base-pair binding pocket.
- To investigate the in vivo consequences of altered DNA polymerase fidelity, specifically the L561A variant.
Main Methods:
- Transient-state kinetic assays using rapid chemical quench to measure dNMP incorporation.
- Determination of kinetic parameters (k(pol) and K(D)) for correct and incorrect dNMP incorporation.
- In vivo mutation frequency analysis using T4 phage infection of Escherichia coli.
Main Results:
- The RB69 pol L561A variant showed significantly increased incorporation efficiency for mispaired bases compared to the wild-type enzyme.
- The L561A variant exhibited a weak mutator phenotype when exonuclease-proficient.
- An exonuclease-deficient L561A variant caused a dominant-lethal phenotype in T4 phage infections, suggesting error catastrophe.
Conclusions:
- Single-site mutations in the nascent base-pair binding pocket of RB69 pol can significantly reduce base selectivity.
- The loss of fidelity in RB69 pol L561A contributes to increased mutation rates.
- The combination of reduced polymerase fidelity and lack of exonuclease activity leads to error catastrophe and lethality.
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