NDLI: Mismatch repair in Escherichia coli enhances instability of (CTG)n triplet repeats from human hereditary diseases.

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Mismatch repair in Escherichia coli enhances instability of (CTG)n triplet repeats from human hereditary diseases.

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Mismatch repair in Escherichia coli enhances instability of (CTG)n triplet repeats from human hereditary diseases.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shimizu, M. Gellibolian, R. Sinden, R. R. Wells, R. D. Kang, S. Bowater, R. P. Jaworski, A. Rosche, W. A.
Description	Author Affiliation: Jaworski A ( Center for Genome Research, Texas A&M University, Texas Medical Center, Houston 77030-3303, USA.);
Abstract	Long CTG triplet repeats which are associated with several human hereditary neuromuscular disease genes are stabilized in ColE1-derived plasmids in Escherichia coli containing mutations in the methyl-directed mismatch repair genes (mutS, mutL, or mutH). When plasmids containing (CTG)180 were grown for about 100 generations in mutS, mutL, or mutH strains, 60-85% of the plasmids contained a full-length repeat, whereas in the parent strain only about 20% of the plasmids contained the full-length repeat. The deletions occur only in the (CTG)180 insert, not in DNA flanking the repeat. While many products of the deletions are heterogeneous in length, preferential deletion products of about 140, 100, 60, and 20 repeats were observed. We propose that the E. coli mismatch repair proteins recognize three-base loops formed during replication and then generate long single-stranded gaps where stable hairpin structures may form which can be bypassed by DNA polymerase during the resynthesis of duplex DNA. Similar studies were conducted with plasmids containing CGG repeats; no stabilization of these triplets was found in the mismatch repair mutants. Since prokaryotic and human mismatch repair proteins are similar, and since several carcinoma cell lines which are defective in mismatch repair show instability of simple DNA microsatellites, these mechanistic investigations in a bacterial cell may provide insights into the molecular basis for some human genetic diseases.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	92
Language	English
Publisher	National Academy of Sciences
Publisher Date	1995-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenosine Triphosphatases DNA Repair Enzymes DNA Repair Escherichia Coli Proteins Escherichia Coli Genetics Trinucleotide Repeats Bacterial Proteins Physiology DNA Replication DNA, Bacterial Biosynthesis DNA-Binding Proteins Endodeoxyribonucleases MutS DNA Mismatch-Binding Protein Rec A Recombinases Metabolism Sequence Deletion Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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