| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print June 26, 2002
Center for Genome Research, Institute of Biosciences & Technology, Houston, TX 77030
Corresponding Author: rwells{at}ibt.tamu.edu
Homologous recombination was shown to enable the expansion of CTG•CAG repeat sequences. Other prior investigations revealed the involvement of replication and DNA repair in these genetic instabilities. Herein, we used a genetic assay to measure the frequency of homologous intermolecular recombination between two CTG•CAG tracts. When compared with non-repeating sequences of similar lengths, long (CTG•CAG)n repeats recombine with a ~60 fold higher frequency. Sequence polymorphisms which interrupt the homogeneity of the CTG•CAG repeat tracts reduce the recombination frequency as compared to the pure uninterrupted repeats. The orientation of the repeats relative to the origin of replication strongly influenced the recombination frequency. This suggests the involvement of DNA replication in the recombination process of triplet repeats. We propose that DNA polymerases stall within the CTG•CAG repeat tracts causing nicks or double strand breaks which stimulate homologous recombination. The recombination process is RecA dependent.
J. Biol. Chem, 10.1074/jbc.M202127200
Submitted on March 4, 2002
Revised on May 31, 2002
Accepted on June 25, 2002
Long CTG•CAG repeats from myotonic dystrophy are preferred sites for intermolecular recombination
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  R. D. Wells DNA triplexes and Friedreich ataxia FASEB J, June 1, 2008; 22(6): 1625 - 1634. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. M. Pollard, R. L. Bourn, and S. I. Bidichandani Repair of DNA double-strand breaks within the (GAA*TTC)n sequence results in frequent deletion of the triplet-repeat sequence Nucleic Acids Res., February 2, 2008; 36(2): 489 - 500. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. M. Pollard, Y. K. Chutake, P. M. Rindler, and S. I. Bidichandani Deficiency of RecA-dependent RecFOR and RecBCD pathways causes increased instability of the (GAA{middle dot}TTC)n sequence when GAA is the lagging strand template Nucleic Acids Res., November 29, 2007; 35(20): 6884 - 6894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Zahra, J. K. Blackwood, J. Sales, and D. R. F. Leach Proofreading and Secondary Structure Processing Determine the Orientation Dependence of CAG{middle dot}CTG Trinucleotide Repeat Instability in Escherichia coli Genetics, May 1, 2007; 176(1): 27 - 41. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Napierala, A. Bacolla, and R. D. Wells Increased Negative Superhelical Density in Vivo Enhances the Genetic Instability of Triplet Repeat Sequences J. Biol. Chem., November 11, 2005; 280(45): 37366 - 37376. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Wells, R. Dere, M. L. Hebert, M. Napierala, and L. S. Son Advances in mechanisms of genetic instability related to hereditary neurological diseases Nucleic Acids Res., July 8, 2005; 33(12): 3785 - 3798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Wojciechowska, A. Bacolla, J. E. Larson, and R. D. Wells The Myotonic Dystrophy Type 1 Triplet Repeat Sequence Induces Gross Deletions and Inversions J. Biol. Chem., January 14, 2005; 280(2): 941 - 952. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I.V. Kovtun, A.R. Thornhill, and C.T. McMurray Somatic deletion events occur during early embryonic development and modify the extent of CAG expansion in subsequent generations Hum. Mol. Genet., December 15, 2004; 13(24): 3057 - 3068. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Dere, M. Napierala, L. P. W. Ranum, and R. D. Wells Hairpin Structure-forming Propensity of the (CCTG{middle dot}CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2 J. Biol. Chem., October 1, 2004; 279(40): 41715 - 41726. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kunnimalaiyaan, R. Kruger, W. Ross, S. A. Rakowski, and M. Filutowicz Binding Modes of the Initiator and Inhibitor Forms of the Replication Protein {pi} to the {gamma} ori Iteron of Plasmid R6K J. Biol. Chem., September 24, 2004; 279(39): 41058 - 41066. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Wang and K. M. Vasquez Naturally occurring H-DNA-forming sequences are mutagenic in mammalian cells PNAS, September 14, 2004; 101(37): 13448 - 13453. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Napierala, R. Dere, A. Vetcher, and R. D. Wells Structure-dependent Recombination Hot Spot Activity of GAA{middle dot}TTC Sequences from Intron 1 of the Friedreich's Ataxia Gene J. Biol. Chem., February 20, 2004; 279(8): 6444 - 6454. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Gorbunova, A. Seluanov, V. Dion, Z. Sandor, J. L. Meservy, and J. H. Wilson Selectable System for Monitoring the Instability of CTG/CAG Triplet Repeats in Mammalian Cells Mol. Cell. Biol., July 1, 2003; 23(13): 4485 - 4493. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Meservy, R. G. Sargent, R. R. Iyer, F. Chan, G. J. McKenzie, R. D. Wells, and J. H. Wilson Long CTG Tracts from the Myotonic Dystrophy Gene Induce Deletions and Rearrangements during Recombination at the APRT Locus in CHO Cells Mol. Cell. Biol., May 1, 2003; 23(9): 3152 - 3162. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Napierala, P. Parniewski, A. Pluciennik, and R. D. Wells Long CTG{middle dot}CAG Repeat Sequences Markedly Stimulate Intramolecular Recombination J. Biol. Chem., September 6, 2002; 277(37): 34087 - 34100. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
