Suppression of gene amplification and chromosomal DNA integration by the DNA mismatch repair system
Source: Nucleic Acids Research, Volume 29, Number 16, 15 August 2001 , pp. 3304-3310(7)
Publisher: Oxford University Press
Abstract:Mismatch repair (MMR)-deficient cells are shown to produce >15-fold more methotrexate-resistant colonies than MMR normal cells. The increased resistance to methotrexate is primarily due to gene amplification since all the resistant clones contain double-minute chromosomes and increased copy numbers of the DHFR gene. In addition, integration of linearized or retroviral DNAs into chromosomes is also significantly elevated in MMR-deficient cells. These results suggest that in addition to microsatellite instability and homeologous recombination, MMR is also involved in suppression of other genome instabilities such as gene amplification and chromosomal DNA integration.
Document Type: Original Article
Affiliations: 1: MCB, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA and 2: Department of Pharmacology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854, USA
Publication date: 15 August 2001
- Nucleic Acids Research (NAR) is a fully Open Access journal, providing rapid publication of leading edge research into the nucleic acids under the following categories: chemistry, computational biology, genomics, molecular biology, nucleic acid enzymes, RNA and structural biology. There is a Survey and Summary section, and methods papers are published
in NAR Methods Online. Each year the first issue is devoted to biological databases, and a later issue to relevant web-based software resources.