ArticleNucleic acids research2001
A mutation in the primer grip region of HIV-1 reverse transcriptase that confers reduced fidelity of DNA synthesis.
Article in Nucleic acids research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Two Coselected Distal Mutations in HIV-1 Reverse Transcriptase (RT) Alter Susceptibility to Nonnucleoside RT Inhibitors and Nucleoside Analogs.Journal of virology · 2019Article
- Altered error specificity of RNase H-deficient HIV-1 reverse transcriptases during DNA-dependent DNA synthesis.Nucleic acids research · 2013Article
- Interrelationship between HIV-1 fitness and mutation rate.Journal of molecular biology · 2013Article
- Lys66 residue as a determinant of high mismatch extension and misinsertion rates of HIV-1 reverse transcriptase.The FEBS journal · 2012Article
- Retrovolution: HIV-driven evolution of cellular genes and improvement of anticancer drug activation.PLoS genetics · 2012Article
- Extensive mutagenesis of the conserved box E motif in duck hepatitis B virus P protein reveals multiple functions in replication and a common structure with the primer grip in HIV-1 reverse transcriptase.Journal of virology · 2012Article
- The reverse transcriptase encoded by the non-LTR retrotransposon R2 is as error-prone as that encoded by HIV-1.Journal of molecular biology · 2011Article
- K65R and K65A substitutions in HIV-1 reverse transcriptase enhance polymerase fidelity by decreasing both dNTP misinsertion and mispaired primer extension efficiencies.Journal of molecular biology · 2010Article
- The M230L nonnucleoside reverse transcriptase inhibitor resistance mutation in HIV-1 reverse transcriptase impairs enzymatic function and viral replicative capacity.Antimicrobial agents and chemotherapy · 2010Article
- Article
- Solution characterization of [methyl-(13)C]methionine HIV-1 reverse transcriptase by NMR spectroscopy.Antiviral research · 2009Article
- Article
- DNA structure-induced recruitment and activation of the Fanconi anemia pathway protein FANCD2.Molecular and cellular biology · 2007Article
- The cost of replication fidelity in human immunodeficiency virus type 1.Proceedings. Biological sciences · 2007Article
- Adaptive value of high mutation rates of RNA viruses: separating causes from consequences.Journal of virology · 2005Review
- Nucleotide specificity of HIV-1 reverse transcriptases with amino acid substitutions affecting Ala-114.The Biochemical journal · 2005Article
- Increased G-->A transition frequencies displayed by primer grip mutants of human immunodeficiency virus type 1 reverse transcriptase.Journal of virology · 2004Article
- Molecular model of SARS coronavirus polymerase: implications for biochemical functions and drug design.Nucleic acids research · 2003Article
- Influence of reverse transcriptase variants, drugs, and Vpr on human immunodeficiency virus type 1 mutant frequencies.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A compensatory mutation (M230I) in the primer grip of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) restores the replication capacity of virus having a Y115W mutation in their RT coding region. The Y115W substitution impairs DNA polymerase activity and produces an enzyme with a lower fidelity of DNA synthesis. Gel-based fidelity assays with the double mutant Y115W/M230I revealed that the M230I substitution increased the accuracy of mutant Y115W. Y115W/M230I showed wild-type misinsertion fidelity in assays performed with DNA/DNA templates. However, when present alone, M230I conferred reduced fidelity as determined in misinsertion and mispair extension fidelity assays, as well as in primer extension assays carried out with three dNTPs. The mutant M230I showed a 3.3-16-fold increase in misinsertion efficiency for G, C and T opposite T, compared with the wild-type enzyme. Its fidelity was not influenced by nucleotide substitutions in the template/primer around the incorporation site. However, its accuracy was apparently affected by the structure of the 5'-overhang of the template strand. Unlike wild-type HIV-1 RT, nucleotide selectivity of mutant M230I at dT:dG, dT:dC and dT:dT mispairs was almost exclusively dependent on the K(m) values for correct and incorrect dNTPs, a characteristic that has not been described for other low fidelity mutants of HIV-1 RT.
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