The S. cerevisiae Mag1 3-methyladenine DNA glycosylase modulates susceptibility to homologous recombination

Hendricks, Carrie A.; Razlog, M.; Matsuguchi, Tetsuya; Goyal, Anish K.; Brock, A.L.; Engelward, Bevin P.

doi:10.1016/s1568-7864(02)00072-1

Cited by 28 publications

(30 citation statements)

References 68 publications

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“…A role of components of other repair pathways, such as BER, in the HR process or in the formation of secondary substrate cannot be excluded (Hendricks et al, 2002). However, our profiling experiments did not reveal any significant changes in expression of genes known to be involved in the BER process.…”

Section: Why Do Atcen2 Plants Exhibit a Hyperrecombinogenic Phenotype?mentioning

confidence: 54%

“…A direct involvement of RAD1 (NER) or MSH2 (MMR) in the HR process has been demonstrated (Liang et al, 1998;Pâ ques and Haber, 1999;Elliott and Jasin, 2001;Villemure et al, 2003). Deregulation of an upstream step of the BER pathway in yeast has been documented to indirectly influence recombinational DNA repair (Hendricks et al, 2002). In bacteria, yeast, and mammals, a combination of NER and HR was shown to be required for inter/intrastrand cross-link repair; inter/intrastrand cross-link removal is performed by the NER machinery, whereas the resulting secondary repair substrates, DSBs, can be repaired by HR (Cole and Sinden, 1975;Jachymczyk et al, 1981;De Silva et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

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CENTRIN2 Modulates Homologous Recombination and Nucleotide Excision Repair in Arabidopsis[W]

et al. 2004

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A genetic screen of a population of Arabidopsis thaliana lines exhibiting enhanced somatic homologous recombination yielded a mutant affected in expression of a gene encoding a caltractin-like protein (centrin). The hyperrecombinogenic phenotype could be reproduced using RNA interference (RNAi) technology. Both the original mutant and the RNAi plants exhibited a moderate UV-C sensitivity as well as a reduced efficiency of in vitro repair of UV-damaged DNA. Transcription profiling of the mutant showed that expression of components of the nucleotide excision repair (NER) pathway and of factors involved in other DNA repair processes were significantly changed. Our data suggest an indirect involvement of centrin in recombinational DNA repair via the modulation of the NER pathway. These findings thus point to a novel interconnection between an early step of NER and homologous recombination, which may play a critical role in plant DNA repair.

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Section: Why Do Atcen2 Plants Exhibit a Hyperrecombinogenic Phenotype?mentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

CENTRIN2 Modulates Homologous Recombination and Nucleotide Excision Repair in Arabidopsis[W]

et al. 2004

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“…This action of Ape1 may be promoted to avert error-prone bypass synthesis and instead create a one-ended DSB (following incision) that can be faithfully resolved by homologous recombination (HR) 36 . A role for HR in AP site repair is supported by genetic evidence in bacteria and yeast [37][38][39] . Alternatively, in the absence of AP site cleavage, or bypass synthesis, the leading DNA strand could be displaced (or degraded) to permit re-annealing of the downstream DNA, ultimately permitting classic template-driven BER prior to the resumption of replicative synthesis.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Abasic Endonuclease Activity of Human Ape1 on Alternative Substrates, as Well as Effects of ATP and Sequence Context on AP Site Incision

Berquist

McNeill

Wilson

2008

Journal of Molecular Biology

107

114

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Human Ape1 is a multifunctional protein with a major role in initiating repair of apurinic/ apyrimidinic (AP) sites in DNA by catalyzing hydrolytic incision of the phosphodiester backbone immediately adjacent to the damage. Besides in double-stranded DNA, Ape1 has been shown to cleave at AP sites in single-stranded (ss) regions of a number of biologically-relevant DNA conformations and in structured ssDNA. Extension of these studies has revealed a more expansive repertoire of model substrates on which Ape1 exerts AP endonuclease activity. In particular, Ape1 possesses the ability to cleave at AP sites located in (i) the DNA strand of a DNA/RNA hybrid, (ii) "pseudo-triplex" bubble substrates designed to mimic stalled replication or transcription intermediates, and (iii) configurations that emulate R-loop structures that arise during class switch recombination (CSR). Moreover, Ape1 was found to cleave AP site-containing ssRNA, suggesting a novel "cleansing" function that may contribute to the elimination of detrimental cellular AP-RNA molecules. Finally, sequence context immediately surrounding an abasic site in duplex DNA was found to have a < 3-fold effect on the incision efficiency of Ape1, and ATP was found to exert complex effects on the endonuclease capacity of Ape1 on double-stranded substrates. The results suggest that in addition to abasic sites in conventional duplex genomic DNA, Ape1 has the ability to incise at AP sites in DNA conformations formed during DNA replication, transcription and CSR, and that Ape1 can endonucleolyticly destroy damaged RNA.

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“…1). It is well known that the initial steps of BER to remove alkylation damage can lead to recombination in E. coli (25,26), yeast (27,28), and mammalian cells (29). However, it has also been shown that de novo protein synthesis is required for AID-induced CSR, and this was interpreted in favor of an RNA-editing model for AID involvement in recombination (30), rather than a DNA repair-linked model.…”

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confidence: 99%

Recombinogenic Phenotype of Human Activation-Induced Cytosine Deaminase

Poltoratsky

Wilson

Kunkel

et al. 2004

The Journal of Immunology

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Class switch recombination, gene conversion, and somatic hypermutation that diversify rearranged Ig genes to produce various classes of high affinity Abs are dependent on the enzyme activation-induced cytosine deaminase (AID). Evidence suggests that somatic hypermutation is due to error-prone DNA repair that is initiated by AID-mediated deamination of cytosine in DNA, whereas the mechanism by which AID controls recombination remains to be elucidated. In this study, using a yeast model system, we have observed AID-dependent recombination. Expression of human AID in wild-type yeast is mutagenic for G-C to A-T transitions, and as expected, this mutagenesis is increased upon inactivation of uracil-DNA glycosylase. AID expression also strongly induces intragenic mitotic recombination, but only in a strain possessing uracil-DNA glycosylase. Thus, the initial step of base excision repair is required for AID-dependent recombination and is a branch point for either hypermutagenesis or recombination.

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The S. cerevisiae Mag1 3-methyladenine DNA glycosylase modulates susceptibility to homologous recombination

Cited by 28 publications

References 68 publications

CENTRIN2 Modulates Homologous Recombination and Nucleotide Excision Repair in Arabidopsis[W]

CENTRIN2 Modulates Homologous Recombination and Nucleotide Excision Repair in Arabidopsis[W]

Characterization of Abasic Endonuclease Activity of Human Ape1 on Alternative Substrates, as Well as Effects of ATP and Sequence Context on AP Site Incision

Recombinogenic Phenotype of Human Activation-Induced Cytosine Deaminase

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