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Relevant bibliographies by topics / Trinucleotide repeat instability

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Academic literature on the topic 'Trinucleotide repeat instability'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Trinucleotide repeat instability"

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Miret, J. J., L. Pessoa-Brandão, and R. S. Lahue. "Instability of CAG and CTG trinucleotide repeats in Saccharomyces cerevisiae." Molecular and Cellular Biology 17, no. 6 (1997): 3382–87. http://dx.doi.org/10.1128/mcb.17.6.3382.

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A quantitative genetic assay was developed to monitor alterations in tract lengths of trinucleotide repeat sequences in Saccharomyces cerevisiae. Insertion of (CAG)50 or (CTG)50 repeats into a promoter that drives expression of the reporter gene ADE8 results in loss of expression and white colony color. Contractions within the trinucleotide sequences to repeat lengths of 8 to 38 restore functional expression of the reporter, leading to red colony color. Reporter constructs including (CAG)50 or (CTG)50 repeat sequences were integrated into the yeast genome, and the rate of red colony formation

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Lahue, Robert S. "DNA repair and trinucleotide repeat instability." Frontiers in Bioscience 8, no. 6 (2003): s653–665. http://dx.doi.org/10.2741/1107.

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Nelson, David L., and Stephen T. Warren. "Trinucleotide repeat instability: when and where?" Nature Genetics 4, no. 2 (1993): 107–8. http://dx.doi.org/10.1038/ng0693-107.

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Cohen, Haim, Dorothy D. Sears, Drora Zenvirth, Philip Hieter, and Giora Simchen. "Increased Instability of Human CTG Repeat Tracts on Yeast Artificial Chromosomes during Gametogenesis." Molecular and Cellular Biology 19, no. 6 (1999): 4153–58. http://dx.doi.org/10.1128/mcb.19.6.4153.

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ABSTRACT Expansion of trinucleotide repeat tracts has been shown to be associated with numerous human diseases. The mechanism and timing of the expansion events are poorly understood, however. We show that CTG repeats, associated with the human DMPK gene and implanted in two homologous yeast artificial chromosomes (YACs), are very unstable. The instability is 6 to 10 times more pronounced in meiosis than during mitotic division. The influence of meiosis on instability is 4.4 times greater when the second YAC with a repeat tract is not present. Most of the changes we observed in trinucleotide r

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Pepers, B. A., J. T. den Dunnen, G.-J. B. van Ommen, and W. M. C. van Roon-Mom. "C01 Trinucleotide repeat instability in Huntington's disease." Journal of Neurology, Neurosurgery & Psychiatry 81, Suppl 1 (2010): A16.1—A16. http://dx.doi.org/10.1136/jnnp.2010.222588.1.

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Kovtun, Irina V., and Cynthia T. McMurray. "Features of trinucleotide repeat instability in vivo." Cell Research 18, no. 1 (2008): 198–213. http://dx.doi.org/10.1038/cr.2008.5.

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Guo, Jinzhen, Luping Chen, and Guo-Min Li. "DNA mismatch repair in trinucleotide repeat instability." Science China Life Sciences 60, no. 10 (2017): 1087–92. http://dx.doi.org/10.1007/s11427-017-9186-7.

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Maurer, D. J., B. L. O'Callaghan, and D. M. Livingston. "Orientation dependence of trinucleotide CAG repeat instability in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 12 (1996): 6617–22. http://dx.doi.org/10.1128/mcb.16.12.6617.

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To examine the chromosomal stability of repetitions of the trinucleotide CAG, we have cloned CAG repeat tracts onto the 3' end of the Saccharomyces cerevisiae ADE2 gene and placed the appended gene into the ARO2 locus of chromosome VII. Examination of chromosomal DNA from sibling colonies arising from clonal expansion of strains harboring repeat tracts showed that repeat tracts often change in length. Most changes in tract length are decreases, but rare increases also occur. Longer tracts are more unstable than smaller tracts. The most unstable tracts, of 80 to 90 repeats, undergo changes at r

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Rolfsmeier, Michael L., Michael J. Dixon, Luis Pessoa-Brandão, Richard Pelletier, Juan José Miret, and Robert S. Lahue. "Cis-Elements Governing Trinucleotide Repeat Instability in Saccharomyces cerevisiae." Genetics 157, no. 4 (2001): 1569–79. http://dx.doi.org/10.1093/genetics/157.4.1569.

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Abstract Trinucleotide repeat (TNR) instability in humans is governed by unique cis-elements. One element is a threshold, or minimal repeat length, conferring frequent mutations. Since thresholds have not been directly demonstrated in model systems, their molecular nature remains uncertain. Another element is sequence specificity. Unstable TNR sequences are almost always CNG, whose hairpin-forming ability is thought to promote instability by inhibiting DNA repair. To understand these cis-elements further, TNR expansions and contractions were monitored by yeast genetic assays. A threshold of ∼1

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McMurray, Cynthia T. "Mechanisms of trinucleotide repeat instability during human development." Nature Reviews Genetics 11, no. 11 (2010): 786–99. http://dx.doi.org/10.1038/nrg2828.

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Dissertations / Theses on the topic "Trinucleotide repeat instability"

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Gadgil, Rujuta Yashodhan. "Instability at Trinucleotide Repeat DNAs." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1472231204.

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Schmidt, Kristina H. "CTG trinucleotide repeat instability in Escherichia coli." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/14353.

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In order to identify cellular factors that affect trinucleotide repeat stability, changes in the length of a (CTG)<sub>43</sub> repeat were studied over 140 generations in wild-type <i>Escherichia coli</i> and in strains that are deficient in post-replicative mismatch repair, secondary structure repair and homologous recombination. It is shown that (CTG)<sub>43</sub> inserted into pUC18 expands and contracts in wild-type <i>E. coli</i> in an orientation-dependent manner that is unaffected by transcription. In cells deficient in post-replicative mismatch repair (CTG)<sub>43</sub> repeat instabi

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Zahra, Rabaab. "CAG.CTG trinucleotide repeat instability in the E.coli chromosome." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/11667.

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In order to identify the molecular basis of genetic instability, a polymerization-independent strategy is developed to generate expanded repeat arrays. The repeat tracts are integrated in the 5’end of <i>lacZ</i> gene in the <i>Escherichia coli</i> chromosome. Using this model system, instability is studied in wild type <i>E. coli</i> and in strains deficient in cellular pathways such as DNA repair, replication and recombination. The work demonstrates that instability (expansion and contraction) in wild type cells is length and orientation dependent. Longer tracts are more unstable than shorte

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Chan, Kara Y. "MECHANISMS OF TRINUCLEOTIDE REPEAT INSTABILITY DURING DNA SYNTHESIS." UKnowledge, 2019. https://uknowledge.uky.edu/toxicology_etds/29.

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Genomic instability, in the form of gene mutations, insertions/deletions, and gene amplifications, is one of the hallmarks in many types of cancers and other inheritable genetic disorders. Trinucleotide repeat (TNR) disorders, such as Huntington’s disease (HD) and Myotonic dystrophy (DM) can be inherited and repeats may be extended through subsequent generations. However, it is not clear how the CAG repeats expand through generations in HD. Two possible repeat expansion mechanisms include: 1) polymerase mediated repeat extension; 2) persistent TNR hairpin structure formation persisting in the

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Warner, Stuart A. "Roles of recombination in trinucleotide repeat instability in E.coli." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/13211.

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Ren, Yaou. "Trinucleotide Repeat Instability Modulated by DNA Repair Enzymes and Cofactors." FIU Digital Commons, 2018. https://digitalcommons.fiu.edu/etd/3762.

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Trinucleotide repeat (TNR) instability including repeat expansions and repeat deletions is the cause of more than 40 inherited incurable neurodegenerative diseases and cancer. TNR instability is associated with DNA damage and base excision repair (BER). In this dissertation research, we explored the mechanisms of BER-mediated TNR instability via biochemical analysis of the BER protein activities, DNA structures, protein-protein interaction, and protein-DNA interaction by reconstructing BER in vitro using synthesized oligonucleotide TNR substrates and purified human proteins. First, we evaluate

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Mihaescu, Camelia. "Investigation of trinucleotide repeat instability in the Escherichia coli chromosome." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/12655.

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The expansion of trinucleotide repeat tracts is the cause of nearly twenty genetic disorders. Almost all these diseases are characterised by anticipation, which means an earlier age of onset and an increased severity of the symptoms from one generation to the next. The mechanisms of trinucleotide repeat expansion are not understood. In the course of this project, I have investigated the instability of a trinucleotide repeat array of 43 copies integrated at the <i>attB </i>site of chromosomes of various <i>Escherichia coli </i>mutants. The trinucleotide repeat tract (CTG)<sub>43 </sub>was integ

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Beaver, Jill M. "Trinucleotide Repeat Instability is Modulated by DNA Base Lesions and DNA Base Excision Repair." FIU Digital Commons, 2016. http://digitalcommons.fiu.edu/etd/3056.

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Trinucleotide repeat (TNR) expansions are the cause of over 40 human neurodegenerative diseases, and are linked to DNA damage and base excision repair (BER). We explored the role of DNA damage and BER in modulating TNR instability through analysis of DNA structures, BER protein activities, and reconstitution of repair using human BER proteins and synthesized DNA containing various types of damage. We show that DNA damage and BER can modulate TNR expansions by promoting removal of a TNR hairpin through coordinated activities of BER proteins and cofactors. We found that during repair in a TNR ha

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Xu, Meng. "Oxidative DNA Damage Modulates Trinucleotide Repeat Instability Via DNA Base Excision Repair." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1576.

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Trinucleotide repeat (TNR) expansion is the cause of more than 40 types of human neurodegenerative diseases such as Huntington’s disease. Recent studies have linked TNR expansion with oxidative DNA damage and base excision repair (BER). In this research, we provided the first evidence that oxidative DNA damage can induce CAG repeat deletion/contraction via BER. We found that BER of an oxidized DNA base lesion, 8-oxoguanine in a CAG repeat tract, resulted in the formation of a CTG hairpin at the template strand. DNA polymerase β (pol b) then skipped over the hairpin creating a 5’-flap that was

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Ueki, Junko. "Myotonic dystrophy type 1 patient-derived iPSCs for the investigation of CTG repeat instability." Kyoto University, 2018. http://hdl.handle.net/2433/230991.

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Book chapters on the topic "Trinucleotide repeat instability"

1

Lai, Yanhao, Ruipeng Lei, Yaou Ren, and Yuan Liu. "Methods to Study Trinucleotide Repeat Instability Induced by DNA Damage and Repair." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9500-4_5.

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Wells, Robert D., Albino Bacolla, and Richard P. Bowater. "Instabilities of Triplet Repeats: Factors and Mechanisms." In Trinucleotide Diseases and Instability. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-540-69680-3_4.

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Deka, Ranjan, and Ranajit Chakraborty. "Trinucleotide Repeats, Genetic Instability and Variation in the Human Genome." In Genomic Diversity. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4263-6_4.

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