Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2000 Oct 10;97(21):11137-9.
doi: 10.1073/pnas.210383397.

DNA damage, DNA repair, cell proliferation, and DNA replication: how do gene mutations result?

J P O'Neill  1
Affiliations

DNA damage, DNA repair, cell proliferation, and DNA replication: how do gene mutations result?

J P O'Neill. Proc Natl Acad Sci U S A. .
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Fate of O6-alkyl G adducts in AGT-deficient cells (G:C→A:T transition mutations). In AGT-proficient cells, the O6-alkyl adduct is removed from G through direct transfer to an acceptor protein. In AGT-deficient cells, there are two possible fates for this and similar adducts. If the cellular DNA is replicated, the O6-alkyl G is misreplicated as an A and a T is incorporated in the new DNA strand. Subsequent replication “fixes” the G:C→A:T mutation (A, mutation in red). This would yield a colony of 50% mutant cells. In the absence of DNA replication, nucleotide excision repair (NER) or base excision repair (BER) processes might recognize the “mismatched” base pair. Correct repair would remove the O6-alkyl G and insert the correct G. Misrepair would remove the C and insert a T opposite O6-alkyl G. The now fixed G:C→A:T mutation would be propagated during subsequent DNA replication (B, mutation in red). The total mutant yield through misrepair would be the same, assuming a 50% probability of either repair or misrepair. However, the mutant colony would be “pure,” i.e., 100% mutant cells.
See this image and copyright information in PMC

Comment on

References

    1. Russell W L, Kelly E M, Hunsicker P R, Bangham J W, Maddux S C, Phipps E L. Proc Natl Acad Sci USA. 1979;76:5818–5819. - PMC - PubMed
    1. Peratoni A O, Rice J M, Reed C D, Watatani M, Wenk M L. Proc Natl Acad Sci USA. 1987;84:6317–6321. - PMC - PubMed
    1. You M, Wang Y, Lineen A M, Gunning W T, Stoner G D, Anderson M W. Carcinogenesis. 1992;13:1583–1586. - PubMed
    1. Bielas J H, Heddle J A. Proc Natl Acad Sci USA. 2000;97:11391–11396. - PMC - PubMed
    1. Heflich R H, Beranek D T, Kodell R L, Morris S M. Mutat Res. 1982;106:147–161. - PubMed

Publication types

LinkOut - more resources