PMID: 9447233Feb 3, 1998Paper

Reversal of methylation tolerance by transfer of human chromosome 2

Mutation Research
G AquilinaM Bignami

Abstract

Human cell lines resistant to N-methyl-N-nitrosourea (MNU) were previously assigned to two complementation groups. Members of group I are defective in mismatch correction [S. Ceccotti, G Aquilina, P. Macpherson, M. Yamada, P. Karran, M. Bignami, Processing of O6-methylguanine by mismatch correction in human cell extracts. Current Biol. 6 (1996) 1528-1531]. To identify the mechanism responsible for the less pronounced phenotype of the second complementation group, we characterized the persistence of MNU-induced O6-methylguanine (O6-meGua) and mutation induction at the hypoxanthine guanine phosphoribosyl-transferase (HPRT) locus. Group II clones are unable to repair the premutagenic base O6-meGua and are as mutable by MNU as group I clones and the parental HeLaMR cells. MNU-induced SCE were undetectable in group I clones and drastically reduced in group II in comparison with the parental cells. These observations are consistent with a defective processing of DNA methylation damage by members of both groups. Group II clones exhibit a moderate spontaneous mutator phenotype at the HPRT gene but significant instability at mononucleotide repeat microsatellites. Introduction of a single human chromosome 2 (but not of chromosome 3 or 7)...Continue Reading

References

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Sep 13, 1994·Proceedings of the National Academy of Sciences of the United States of America·G AquilinaM Bignami
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Citations

Oct 27, 1999·Proceedings of the National Academy of Sciences of the United States of America·D R DuckettP Modrich
Feb 26, 2000·Annual Review of Genetics·A B BuermeyerR M Liskay
Aug 17, 1999·Seminars in Cancer Biology·J Breivik, G Gaudernack

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