The repair of 5-methylcytosine deamination damage

Wiebauer, Karin; Neddermann, Petra; Hughes, Melya J.; Jiricny, Josef

doi:10.1007/978-3-0348-9118-9_23

Cited by 18 publications

(14 citation statements)

References 36 publications

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“…Indeed, although cytosine and 5-methylcytosine undergo comparable rates of spontaneous hydrolytic deamination that respectively produce uridine and thymine, the mismatch repair of C→T transitions is less efficient than that of C→U transitions3435. Therefore, as in many eukaryotic lineages (including plants) DNA methylation is preponderant in repeated sequences36, these have relatively low G+C contents as compared with host genes in various species37.…”

Section: Resultsmentioning

confidence: 99%

Ancestral repeats have shaped epigenome and genome composition for millions of years in Arabidopsis thaliana

Maumus¹,

Quesneville²

2014

Nat Commun

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Little is known about the evolution of repeated sequences over long periods of time. Using two independent approaches, we show that the majority of the repeats found in the Arabidopsis thaliana genome are ancient and likely to derive from the retention of fragments deposited during ancestral bursts that occurred early in the Brassicaceae evolution. We determine that the majority of young repeats are found in pericentromeric domains, while older copies are frequent in the gene-rich regions. Our results further suggest that the DNA methylation of repeats through small RNA-mediated pathways can last over prolonged periods of time. We also illustrate the way repeated sequences are composted by mutations towards genomic dark matter over time, probably driven by the deamination of methylcytosines, which also have an impact on epigenomic landscapes. Overall, we show that the ancient proliferation of repeat families has long-term consequences on A. thaliana biology and genome composition.

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Section: Resultsmentioning

confidence: 99%

Ancestral repeats have shaped epigenome and genome composition for millions of years in Arabidopsis thaliana

Maumus¹,

Quesneville²

2014

Nat Commun

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“…In wild-type (dcm + vsr + ) lysogens, a vsr + plasmid reduced mutation at the 5meC hot-spot about fourfold, showing that VSP repair in wild-type bacteria is limited by the amount of Vsr available (Lieb, 1991). Wiebauer et al (1993) have suggested that long patch repair might occasionally replace the G in a T:G mispair with A, and that this could account for the mutation hot-spots at 5meC in vsr + bacteria. However, correction of G in T:G mispairs in heteroduplex DNA is very rare (< 2%) when the Gcontaining strand is fully methylated (Jones et al, 1987).…”

Section: Vsp Repair and Mutation Avoidancementioning

confidence: 99%

Very short patch repair: reducing the cost of cytosine methylation

Lieb

Bhagwat

1996

Molecular Microbiology

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In Escherichia coli and related bacteria, the product of gene dcm methylates the second cytosine of 5'-CCWGG sequences (where W is A or T). Deamination of 5-methylcytosine (5meC) results in C to T mutations. The mutagenic potential of 5meC is reduced by a system called very short patch (VSP) repair, which replaces T with C. T:G and U:G mispairs in the methylatable sequence and in related sequences are recognized by the product of vsr, a gene adjacent to dcm. Vsr creates a nick just 5' of the mispaired pyrimidine to initiate the repair. Additional products known to be required for VSP repair are DNA polymerase I and DNA ligase. MutS and MutL have a stimulatory role but are not required. The ability of Vsr to recognize T:G mispairs in sequences related to CCWGG is probably responsible for over- and under-representation of certain tetranucleotides in the E. coli genome. Although VSP repair reduces spontaneous mutations at 5meCs in replicating bacteria, mutation hot-spots persist at these sites. Under conditions that more accurately mimic the natural environment of E. coli, VSP repair appears to be effective in preventing mutation at 5meC.

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“…This pathway is characterized by broad mismatch specificity and is believed to be responsible for correcting DNA biosynthetic errors and processing recombination heteroduplexes that contain mismatched base pairs. Short-patch systems, which exhibit restricted mismatch specificity and whose primary function may be processing of particular chemically damaged base pairs (3)(4)(5)(6), are discussed elsewhere (7). Since bacterial mismatch correction has been the subject of several reviews (8-lo), our intent is to briefly discuss the prokaryotic system in order to emphasize results from higher cells.…”

Section: Introductionmentioning

confidence: 99%

Mismatch Repair in Replication Fidelity, Genetic Recombination, and Cancer Biology

Modrich¹,

Lahue²

1996

Annu. Rev. Biochem.

1,377

799

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Mismatch repair stabilizes the cellular genome by correcting DNA replication errors and by blocking recombination events between divergent DNA sequences. The reaction responsible for strand-specific correction of mispaired bases has been highly conserved during evolution, and homologs of bacterial M u 6 and Mu& which play key roles in mismatch recognition and initiation of repair, have been identified in yeast and mammalian cells. Inactivation of genes encoding these activities results in a large increase in spontaneous mutability, and in the case of mice and men, predisposition to tumor development. CONTENTS

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The repair of 5-methylcytosine deamination damage

Cited by 18 publications

References 36 publications

Ancestral repeats have shaped epigenome and genome composition for millions of years in Arabidopsis thaliana

Ancestral repeats have shaped epigenome and genome composition for millions of years in Arabidopsis thaliana

Very short patch repair: reducing the cost of cytosine methylation

Mismatch Repair in Replication Fidelity, Genetic Recombination, and Cancer Biology

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