YtkD and MutT Protect Vegetative Cells but Not Spores of
            <i>Bacillus subtilis</i>
            from Oxidative Stress

Castellanos-Juárez, Francisco X.; Álvarez‐Álvarez, Carlos; Yasbin, Ronald E.; Setlow, Barbara; Setlow, Peter; Pedraza-Reyes, Mario

doi:10.1128/jb.188.6.2285-2289.2006

Cited by 27 publications

(28 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cells deficient for mutT, yvcI, or yjhB showed virtually no change in mutation frequency relative to a wild-type strain; a similar result occurred when all three genes were disrupted (355,356). There is evidence suggesting that the ytkD gene may encode an activity that is similar to that of E. coli MutT (55,324,428). It was shown that YtkD can specifically hydrolyze 8-oxo-(d)GTP, as well as complement a mutT deficiency in E. coli.…”

Section: The "Go" Systemmentioning

confidence: 60%

See 1 more Smart Citation

DNA Repair and Genome Maintenance in Bacillus subtilis

Lenhart

Schroeder

Walsh

et al. 2012

Microbiol Mol Biol Rev

142

155

View full text Add to dashboard Cite

SUMMARY From microbes to multicellular eukaryotic organisms, all cells contain pathways responsible for genome maintenance. DNA replication allows for the faithful duplication of the genome, whereas DNA repair pathways preserve DNA integrity in response to damage originating from endogenous and exogenous sources. The basic pathways important for DNA replication and repair are often conserved throughout biology. In bacteria, high-fidelity repair is balanced with low-fidelity repair and mutagenesis. Such a balance is important for maintaining viability while providing an opportunity for the advantageous selection of mutations when faced with a changing environment. Over the last decade, studies of DNA repair pathways in bacteria have demonstrated considerable differences between Gram-positive and Gram-negative organisms. Here we review and discuss the DNA repair, genome maintenance, and DNA damage checkpoint pathways of the Gram-positive bacterium Bacillus subtilis. We present their molecular mechanisms and compare the functions and regulation of several pathways with known information on other organisms. We also discuss DNA repair during different growth phases and the developmental program of sporulation. In summary, we present a review of the function, regulation, and molecular mechanisms of DNA repair and mutagenesis in Gram-positive bacteria, with a strong emphasis on B. subtilis.

show abstract

Section: The "Go" Systemmentioning

confidence: 60%

“…It was shown that YtkD can specifically hydrolyze 8-oxo-(d)GTP, as well as complement a mutT deficiency in E. coli. It was also shown that cells deficient for ytkD are more susceptible to oxidative DNA damage (55,324,428). However, others have presented evidence that YtkD fails to hydrolyze 8-oxo-dGTP selectively over dGTP (458).…”

Section: The "Go" Systemmentioning

confidence: 99%

DNA Repair and Genome Maintenance in Bacillus subtilis

Lenhart

Schroeder

Walsh

et al. 2012

Microbiol Mol Biol Rev

142

155

View full text Add to dashboard Cite

show abstract

“…On the other hand, incorporation of 8-oxo-GTP into mRNAs may promote transcriptional mutagenesis (51). B. subtilis relies on the glycosylases MutM and MutY to contend with the potential mutagenic effects of the 8-oxo-G:A mispairing, as well as on the NUDIX proteins YtkD and MutT to prevent the potentially cytotoxic and genotoxic effects of oxidized precursors during DNA and RNA synthesis (10,38,45).…”

Section: In Conclusion Our Results Support the Idea That Mmr Regulatmentioning

confidence: 99%

Mismatch Repair Modulation of MutY Activity Drives Bacillus subtilis Stationary-Phase Mutagenesis

et al. 2011

Self Cite

View full text Add to dashboard Cite

show abstract

“…6B). Additive or synergistic effects on the frequency of mutagenesis can be detected using this assay (11,32). Furthermore, we combined the dnaN5(G73R) allele with the mutS5A allele and determined the mutation frequency.…”

Section: Dnan5(g73r)mentioning

confidence: 99%

Mutations in the Bacillus subtilis β Clamp That Separate Its Roles in DNA Replication from Mismatch Repair

et al. 2010

View full text Add to dashboard Cite

The ␤ clamp is an essential replication sliding clamp required for processive DNA synthesis. The ␤ clamp is also critical for several additional aspects of DNA metabolism, including DNA mismatch repair (MMR). The dnaN5 allele of Bacillus subtilis encodes a mutant form of ␤ clamp containing the G73R substitution. Cells with the dnaN5 allele are temperature sensitive for growth due to a defect in DNA replication at 49°C, and they show an increase in mutation frequency caused by a partial defect in MMR at permissive temperatures. We selected for intragenic suppressors of dnaN5 that rescued viability at 49°C to determine if the DNA replication defect could be separated from the MMR defect. We isolated three intragenic suppressors of dnaN5 that restored growth at the nonpermissive temperature while maintaining an increase in mutation frequency. All three dnaN alleles encoded the G73R substitution along with one of three novel missense mutations. The missense mutations isolated were S22P, S181G, and E346K. Of these, S181G and E346K are located near the hydrophobic cleft of the ␤ clamp, a common site occupied by proteins that bind the ␤ clamp. Using several methods, we show that the increase in mutation frequency resulting from each dnaN allele is linked to a defect in MMR. Moreover, we found that S181G and E346K allowed growth at elevated temperatures and did not have an appreciable effect on mutation frequency when separated from G73R. Thus, we found that specific residue changes in the B. subtilis ␤ clamp separate the role of the ␤ clamp in DNA replication from its role in MMR.Replication sliding clamps are essential cellular proteins imparting a spectacular degree of processivity to DNA polymerases during genome replication (24,(39)(40)(41). Encoded by the dnaN gene, the ␤ clamp is a highly conserved bacterial sliding clamp found in virtually all eubacterial species (reviewed in reference 7). The ␤ clamp is a head-to-tail, ringshaped homodimer that encircles double-stranded DNA (1, 39). In eukaryotes and archaea, the analog of the ␤ clamp is proliferating cell nuclear antigen (PCNA) (15,28,40,41). Eukaryotic PCNA is a ring-shaped homotrimer that also acts to encircle DNA, increasing the processivity of the replicative DNA polymerases (40,41). Although the primary structures of the ␤ clamp and PCNA are not conserved, the tertiary structures of these proteins are very similar, demonstrating structural conservation among bacterial, archaeal, and eukaryotic replication sliding clamps (28, 39-41; reviewed in reference 6).The function of the ␤ clamp is not limited to its well-defined role in genome replication. The Escherichia coli ␤ clamp binds Hda, which also binds the replication initiation protein DnaA, regulating the active form of DnaA complexed with ATP (19,37,43). This allows the ␤ clamp to regulate replication initiation through the amount of available DnaA-ATP. In Bacillus subtilis, the ␤ clamp binds YabA, a negative regulator of DNA replication initiation (12,29,52). It has also been suggested that the B. subt...

show abstract

YtkD and MutT Protect Vegetative Cells but Not Spores of Bacillus subtilis from Oxidative Stress

Cited by 27 publications

References 31 publications

DNA Repair and Genome Maintenance in Bacillus subtilis

DNA Repair and Genome Maintenance in Bacillus subtilis

Mismatch Repair Modulation of MutY Activity Drives Bacillus subtilis Stationary-Phase Mutagenesis

Mutations in the Bacillus subtilis β Clamp That Separate Its Roles in DNA Replication from Mismatch Repair

Contact Info

Product

Resources

About