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A specific mismatch repair event protects mammalian cells from loss of 5-methylcytosine


Brown, T C; Jiricny, J (1987). A specific mismatch repair event protects mammalian cells from loss of 5-methylcytosine. Cell, 50(6):945-950.

Abstract

5-Methylcytosine spontaneously deaminates to form thymine, thus generating G/T mispairs in DNA. We investigated the way in which these lesions are addressed in mammalian cells by introducing specific G/T mispairs into the genome of SV40 and determining the fate of the mismatched bases in simian cells. Mispairs were incorporated in 12 bp synthetic duplexes ligated into SV40 DNA between the BstXI and TaqI restriction sites. Analysis of 347 plaques obtained after transfection of this modified DNA indicated that mispairs were corrected in 343 cases (99%), revealing 314 repair events in favor of guanine (90%) and 29 in favor of thymine (8%). Correction in favor of guanine occurred regardless of the orientation of the mispair in DNA and regardless of whether the mispair was in the commonly methylated CpG dinucleotide. These results attest to a specific mismatch repair pathway that restores G/C pairs lost through deamination of 5-methylcytosine residues.

Abstract

5-Methylcytosine spontaneously deaminates to form thymine, thus generating G/T mispairs in DNA. We investigated the way in which these lesions are addressed in mammalian cells by introducing specific G/T mispairs into the genome of SV40 and determining the fate of the mismatched bases in simian cells. Mispairs were incorporated in 12 bp synthetic duplexes ligated into SV40 DNA between the BstXI and TaqI restriction sites. Analysis of 347 plaques obtained after transfection of this modified DNA indicated that mispairs were corrected in 343 cases (99%), revealing 314 repair events in favor of guanine (90%) and 29 in favor of thymine (8%). Correction in favor of guanine occurred regardless of the orientation of the mispair in DNA and regardless of whether the mispair was in the commonly methylated CpG dinucleotide. These results attest to a specific mismatch repair pathway that restores G/C pairs lost through deamination of 5-methylcytosine residues.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Molecular Cancer Research
07 Faculty of Science > Institute of Molecular Cancer Research
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:1987
Deposited On:09 Jul 2010 08:55
Last Modified:21 Feb 2018 11:51
Publisher:Elsevier
ISSN:0092-8674
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/0092-8674(87)90521-6
PubMed ID:3040266

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