Relevant bibliographies by topics / Repeat instabilty

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Academic literature on the topic 'Repeat instabilty'

Author: Grafiati
Published: 19 October 2024

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Journal articles on the topic "Repeat instabilty"

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Khristich, Alexandra N., and Sergei M. Mirkin. "On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability." Journal of Biological Chemistry 295, no. 13 (2020): 4134–70. http://dx.doi.org/10.1074/jbc.rev119.007678.

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Expansions of simple tandem repeats are responsible for almost 50 human diseases, the majority of which are severe, degenerative, and not currently treatable or preventable. In this review, we first describe the molecular mechanisms of repeat-induced toxicity, which is the connecting link between repeat expansions and pathology. We then survey alternative DNA structures that are formed by expandable repeats and review the evidence that formation of these structures is at the core of repeat instability. Next, we describe the consequences of the presence of long structure-forming repeats at the molecular level: somatic and intergenerational instability, fragility, and repeat-induced mutagenesis. We discuss the reasons for gender bias in intergenerational repeat instability and the tissue specificity of somatic repeat instability. We also review the known pathways in which DNA replication, transcription, DNA repair, and chromatin state interact and thereby promote repeat instability. We then discuss possible reasons for the persistence of disease-causing DNA repeats in the genome. We describe evidence suggesting that these repeats are a payoff for the advantages of having abundant simple-sequence repeats for eukaryotic genome function and evolvability. Finally, we discuss two unresolved fundamental questions: (i) why does repeat behavior differ between model systems and human pedigrees, and (ii) can we use current knowledge on repeat instability mechanisms to cure repeat expansion diseases?
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Lin, Yunfu, and John H. Wilson. "Transcription-Induced CAG Repeat Contraction in Human Cells Is Mediated in Part by Transcription-Coupled Nucleotide Excision Repair." Molecular and Cellular Biology 27, no. 17 (2007): 6209–17. http://dx.doi.org/10.1128/mcb.00739-07.

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ABSTRACT Expansions of CAG repeat tracts in the germ line underlie several neurological diseases. In human patients and mouse models, CAG repeat tracts display an ongoing instability in neurons, which may exacerbate disease symptoms. It is unclear how repeats are destabilized in nondividing cells, but it cannot involve DNA replication. We showed previously that transcription through CAG repeats induces their instability (Y. Lin, V. Dion, and J. H. Wilson, Nat. Struct. Mol. Biol. 13:179-180). Here, we present a genetic analysis of the link between transcription-induced repeat instability and nucleotide excision repair (NER) in human cells. We show that short interfering RNA-mediated knockdown of CSB, a component specifically required for transcription-coupled NER (TC-NER), and knockdowns of ERCC1 and XPG, which incise DNA adjacent to damage, stabilize CAG repeat tracts. These results suggest that TC-NER is involved in the pathway for transcription-induced CAG repeat instability. In contrast, knockdowns of OGG1 and APEX1, key components involved in base excision repair, did not affect repeat instability. In addition, repeats are stabilized by knockdown of transcription factor IIS, consistent with a requirement for RNA polymerase II (RNAPII) to backtrack from a transcription block. Repeats also are stabilized by knockdown of either BRCA1 or BARD1, which together function as an E3 ligase that can ubiquitinate arrested RNAPII. Treatment with the proteasome inhibitor MG132, which stabilizes repeats, confirms proteasome involvement. We integrate these observations into a tentative pathway for transcription-induced CAG repeat instability that can account for the contractions observed here and potentially for the contractions and expansions seen with human diseases.
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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 repeat tracts are large contractions of 21 to 50 repeats. The orientation of the insert with the repeats has no effect on the frequency and distribution of the contractions. In our experiments, expansions were found almost exclusively during gametogenesis. Genetic analysis of segregating markers among meiotic progeny excluded unequal crossover as the mechanism for instability. These unique patterns have novel implications for possible mechanisms of repeat instability.
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Brouwer, Judith Rixt, Aline Huguet, Annie Nicole, Arnold Munnich, and Geneviève Gourdon. "Transcriptionally Repressive Chromatin Remodelling and CpG Methylation in the Presence of Expanded CTG-Repeats at the DM1 Locus." Journal of Nucleic Acids 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/567435.

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An expanded CTG-repeat in the 3′ UTR of theDMPKgene is responsible for myotonic dystrophy type I (DM1). Somatic and intergenerational instability cause the disease to become more severe during life and in subsequent generations. Evidence is accumulating that trinucleotide repeat instability and disease progression involve aberrant chromatin dynamics. We explored the chromatin environment in relation to expanded CTG-repeat tracts in hearts from transgenic mice carrying the DM1 locus with different repeat lengths. Using bisulfite sequencing we detected abundant CpG methylation in the regions flanking the expanded CTG-repeat. CpG methylation was postulated to affect CTCF binding but we found that CTCF binding is not affected by CTG-repeat length in our transgenic mice. We detected significantly decreasedDMPKsense andSIX5transcript expression levels in mice with expanded CTG-repeats. Expression of the DM1 antisense transcript was barely affected by CTG-repeat expansion. In line with altered gene expression, ChIP studies revealed a locally less active chromatin conformation around the expanded CTG-repeat, namely, decreased enrichment of active histone mark H3K9/14Ac and increased H3K9Me3 enrichment (repressive chromatin mark). We also observed binding of PCNA around the repeats, a candidate that could launch chromatin remodelling cascades at expanded repeats, ultimately affecting gene transcription and repeat instability.
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Gold, Michaela A., Jenna M. Whalen, Karine Freon, et al. "Restarted replication forks are error-prone and cause CAG repeat expansions and contractions." PLOS Genetics 17, no. 10 (2021): e1009863. http://dx.doi.org/10.1371/journal.pgen.1009863.

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Disease-associated trinucleotide repeats form secondary DNA structures that interfere with replication and repair. Replication has been implicated as a mechanism that can cause repeat expansions and contractions. However, because structure-forming repeats are also replication barriers, it has been unclear whether the instability occurs due to slippage during normal replication progression through the repeat, slippage or misalignment at a replication stall caused by the repeat, or during subsequent replication of the repeat by a restarted fork that has altered properties. In this study, we have specifically addressed the fidelity of a restarted fork as it replicates through a CAG/CTG repeat tract and its effect on repeat instability. To do this, we used a well-characterized site-specific replication fork barrier (RFB) system in fission yeast that creates an inducible and highly efficient stall that is known to restart by recombination-dependent replication (RDR), in combination with long CAG repeat tracts inserted at various distances and orientations with respect to the RFB. We find that replication by the restarted fork exhibits low fidelity through repeat sequences placed 2–7 kb from the RFB, exhibiting elevated levels of Rad52- and Rad8ScRad5/HsHLTF-dependent instability. CAG expansions and contractions are not elevated to the same degree when the tract is just in front or behind the barrier, suggesting that the long-traveling Polδ-Polδ restarted fork, rather than fork reversal or initial D-loop synthesis through the repeat during stalling and restart, is the greatest source of repeat instability. The switch in replication direction that occurs due to replication from a converging fork while the stalled fork is held at the barrier is also a significant contributor to the repeat instability profile. Our results shed light on a long-standing question of how fork stalling and RDR contribute to expansions and contractions of structure-forming trinucleotide repeats, and reveal that tolerance to replication stress by fork restart comes at the cost of increased instability of repetitive sequences.
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Neil, Alexander J., Julia A. Hisey, Ishtiaque Quasem, et al. "Replication-independent instability of Friedreich’s ataxia GAA repeats during chronological aging." Proceedings of the National Academy of Sciences 118, no. 5 (2021): e2013080118. http://dx.doi.org/10.1073/pnas.2013080118.

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Nearly 50 hereditary diseases result from the inheritance of abnormally long repetitive DNA microsatellites. While it was originally believed that the size of inherited repeats is the key factor in disease development, it has become clear that somatic instability of these repeats throughout an individual’s lifetime strongly contributes to disease onset and progression. Importantly, somatic instability is commonly observed in terminally differentiated, postmitotic cells, such as neurons. To unravel the mechanisms of repeat instability in nondividing cells, we created an experimental system to analyze the mutability of Friedreich’s ataxia (GAA)n repeats during chronological aging of quiescent Saccharomyces cerevisiae. Unexpectedly, we found that the predominant repeat-mediated mutation in nondividing cells is large-scale deletions encompassing parts, or the entirety, of the repeat and adjacent regions. These deletions are caused by breakage at the repeat mediated by mismatch repair (MMR) complexes MutSβ and MutLα and DNA endonuclease Rad1, followed by end-resection by Exo1 and repair of the resulting double-strand breaks (DSBs) via nonhomologous end joining. We also observed repeat-mediated gene conversions as a result of DSB repair via ectopic homologous recombination during chronological aging. Repeat expansions accrue during chronological aging as well—particularly in the absence of MMR-induced DSBs. These expansions depend on the processivity of DNA polymerase δ while being counteracted by Exo1 and MutSβ, implicating nick repair. Altogether, these findings show that the mechanisms and types of (GAA)n repeat instability differ dramatically between dividing and nondividing cells, suggesting that distinct repeat-mediated mutations in terminally differentiated somatic cells might influence Friedreich’s ataxia pathogenesis.
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Calluori, Stephanie, Rebecca Stark, and Brandon L. Pearson. "Gene–Environment Interactions in Repeat Expansion Diseases: Mechanisms of Environmentally Induced Repeat Instability." Biomedicines 11, no. 2 (2023): 515. http://dx.doi.org/10.3390/biomedicines11020515.

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Short tandem repeats (STRs) are units of 1–6 base pairs that occur in tandem repetition to form a repeat tract. STRs exhibit repeat instability, which generates expansions or contractions of the repeat tract. Over 50 diseases, primarily affecting the central nervous system and muscles, are characterized by repeat instability. Longer repeat tracts are typically associated with earlier age of onset and increased disease severity. Environmental exposures are suspected to play a role in the pathogenesis of repeat expansion diseases. Here, we review the current knowledge of mechanisms of environmentally induced repeat instability in repeat expansion diseases. The current evidence demonstrates that environmental factors modulate repeat instability via DNA damage and induction of DNA repair pathways, with distinct mechanisms for repeat expansion and contraction. Of particular note, oxidative stress is a key mediator of environmentally induced repeat instability. The preliminary evidence suggests epigenetic modifications as potential mediators of environmentally induced repeat instability. Future research incorporating an array of environmental exposures, new human cohorts, and improved model systems, with a continued focus on cell-types, tissues, and critical windows, will aid in identifying mechanisms of environmentally induced repeat instability. Identifying environmental modulators of repeat instability and their mechanisms of action will inform preventions, therapies, and public health measures.
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Gorbunova, Vera, Andrei Seluanov, Vincent Dion, Zoltan Sandor, James L. Meservy, and John H. Wilson. "Selectable System for Monitoring the Instability of CTG/CAG Triplet Repeats in Mammalian Cells." Molecular and Cellular Biology 23, no. 13 (2003): 4485–93. http://dx.doi.org/10.1128/mcb.23.13.4485-4493.2003.

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ABSTRACT Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide repeats cause neurodegenerative diseases, little is known about the basis for repeat instability itself. By taking advantage of a novel phenomenon, we have developed a selectable assay to detect contractions of CTG/CAG triplets. When inserted into an intron in the APRT gene or the HPRT minigene, long tracts of CTG/CAG repeats (more than about 33 repeat units) are efficiently incorporated into mRNA as a new exon, thereby rendering the encoded protein nonfunctional, whereas short repeat tracts do not affect the phenotype. Therefore, contractions of long repeats can be monitored in large cell populations, by selecting for HPRT+ or APRT+ clones. Using this selectable system, we determined the frequency of spontaneous contractions and showed that treatments with DNA-damaging agents stimulate repeat contractions. The selectable system that we have developed provides a versatile tool for the analysis of CTG/CAG repeat instability in mammalian cells. We also discuss how the effect of long CTG/CAG repeat tracts on splicing may contribute to the progression of polyglutamine diseases.
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Jung, Da Eun, and Chul Hyoung Lyoo. "A Spinocerebellar Ataxia Type 6 Patient Caused by <i>De Novo</i> Expansion of Normal Range CAG Repeats." Journal of the Korean Neurological Association 42, no. 2 (2024): 150–52. http://dx.doi.org/10.17340/jkna.2023.0105.

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Spinocerebellar ataxia type 6 (SCA6) is classified as a CAG repeat disorder, where the number of expanded CAG repeats often undergoes meiotic instability, when transmitted from one generation to the next. However, in SCA6, both normal and expanded CAG repeats tend to remain stable during transmission due to its relatively small repeat numbers. We herein report &lt;i&gt;de-novo&lt;/i&gt; expansion of CAG repeats in SCA6 gene in a 41-year-old female patient, whose parents had normal repeat numbers.
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Su, Xiaofeng A., and Catherine H. Freudenreich. "Cytosine deamination and base excision repair cause R-loop–induced CAG repeat fragility and instability in Saccharomyces cerevisiae." Proceedings of the National Academy of Sciences 114, no. 40 (2017): E8392—E8401. http://dx.doi.org/10.1073/pnas.1711283114.

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CAG/CTG repeats are structure-forming repetitive DNA sequences, and expansion beyond a threshold of ∼35 CAG repeats is the cause of several human diseases. Expanded CAG repeats are prone to breakage, and repair of the breaks can cause repeat contractions and expansions. In this study, we found that cotranscriptional R-loops formed at a CAG-70 repeat inserted into a yeast chromosome. R-loops were further elevated upon deletion of yeast RNaseH genes and caused repeat fragility. A significant increase in CAG repeat contractions was also observed, consistent with previous human cell studies. Deletion of yeast cytosine deaminase Fcy1 significantly decreased the rate of CAG repeat fragility and contractions in the rnh1Δrnh201Δ background, indicating that Fcy1-mediated deamination is one cause of breakage and contractions in the presence of R-loops. Furthermore, base excision repair (BER) is responsible for causing CAG repeat contractions downstream of Fcy1, but not fragility. The Rad1/XPF and Rad2/XPG nucleases were also important in protecting against contractions, but through BER rather than nucleotide excision repair. Surprisingly, the MutLγ (Mlh1/Mlh3) endonuclease caused R-loop–dependent CAG fragility, defining an alternative function for this complex. These findings provide evidence that breakage at expanded CAG repeats occurs due to R-loop formation and reveal two mechanisms for CAG repeat instability: one mediated by cytosine deamination of DNA engaged in R-loops and the other by MutLγ cleavage. Since disease-causing CAG repeats occur in transcribed regions, our results suggest that R-loop–mediated fragility is a mechanism that could cause DNA damage and repeat-length changes in human cells.
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Dissertations / Theses on the topic "Repeat instabilty"

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Pontual, Laure de. "Identification de nouveaux facteurs chimiques capables de moduler l'instabilité des répétitions CTG dans la dystrophie myotonique de type 1." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS198.pdf.

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La dystrophie myotonique de type 1 (DM1) est la dystrophie la plus fréquente chez l'adulte avec une prévalence estimée à 1 : 8000 individus. C'est une maladie multi-systémique caractérisée par des atteintes musculaires, cardiaques, cognitives et digestives responsables d'une réduction de l'espérance et de la qualité de vie des patients. Elle est causée par une expansion anormale de répétitions CTG en 3'UTR du gène DMPK. Dans la population générale, le nombre de répétitions est inférieur à 35 CTG tandis qu'il dépasse 50 CTG et peut atteindre jusqu'à plusieurs milliers de répétitions chez les patients. Comme dans d'autres maladies causées par une expansions de triplets répétés, l'expansion CTG est instable chez les patients DM1. La taille des répétitions CTG augmente entre les générations (instabilité intergénérationnelle) et au sein des tissus au cours de la vie des patients (instabilité somatique). Or, le nombre de répétitions héritées ainsi que le niveau d'instabilité somatique corrèlent avec l'âge d'apparition des symptômes ainsi qu'avec leur sévérité. S'attaquer à la mutation elle-même pour stabiliser ou réduire le nombre de répétitions CTG est la voie thérapeutique la plus prometteuse puisque cela permettrait d'agir sur l'ensemble des mécanismes physiopathologiques qui découlent de la présence de la mutation.Dans un premier temps, mes travaux de thèse ont porté sur l'identification de molécules chimiques de repositionnement capables de moduler l'instabilité des répétitions. Le criblage des 1280 molécules de la chimiothèque Prestwick m'a permis d'identifier 39 molécules candidates qui modifient l'expression d'un gène rapporteur suggérant qu'elles pourraient moduler l'instabilité des répétitions. Après étude directe de leur effet sur l'instabilité, j'ai pu exclure quatre de ces molécules qui ne modulent pas l'expression des répétitions. J'ai montré qu'une cinquième molécule, la clomipramine, était capable de moduler l'instabilité des répétitions dans le modèle cellulaire de criblage mais pas dans des modèles cellulaires DM1 murins et humains.Parallèlement, j'ai démontré que RGFP966, un inhibiteur sélectif d'HDAC3, induisait des contractions des répétitions CTG dans des fibroblastes murins DM1 avec environ 650 répétitions CTG. Cet effet semble dépendre de la dose de RGFP966 ou de la taille de la répétition CTG car il n'a pas été reproduit dans des fibroblastes humains DM1 avec 350 CTG. Une approche RNA-seq dans les cellules murines traitées avec RGFP966 a permis d'identifier plusieurs gènes candidats impliqués dans la réplication de l'ADN, comme modificateurs possibles de l'instabilité. J'ai également montré une diminution de la transcription bidirectionnelle de DMPK associée à une probable hyperméthylation en aval des répétitions dans les cellules murines DM1. En conclusion, mes données suggèrent que RGFP966 module l'instabilité des répétitions CTG dans la DM1 par de multiples mécanismes, incluant potentiellement une modification de la structure chromatinienne au locus DM1 et des altérations de la réplication de l'ADN.L'ensemble de mon projet de thèse a permis de progresser dans la compréhension des mécanismes de l'instabilité et dans l'identification de molécules chimiques modulant la dynamique de l'instabilité. Mes travaux de thèse ont également permis de relever les limites de chacun des modèles utilisés et la complexité d'identifier de petites molécules modifiant la dynamique des triplets CTG en utilisant des modèles cellulaires rapporteurs. Par ailleurs, j'ai participé au développement pour la DM1 du séquençage à longues lectures (avec et sans amplification), un nouvel outil rapide et très informatif pour analyser la mosaïque somatique<br>Myotonic dystrophy type 1 (DM1) is the most common dystrophy in adults, with an estimated prevalence of 1:8000 individuals. It is a multisystemic disease characterized by muscle, cardiac, cognitive, and digestive impairments, which contribute to a reduction in both life expectancy and quality of life for patients. DM1 is caused by an abnormal expansion of CTG repeats in the 3'UTR of the DMPK gene. In the general population, the number of repeats is under 35 CTG, whereas in patients, it exceeds 50 CTG and can reach several thousand repeats. As in other diseases caused by repeat expansions, the CTG expansion in DM1 is unstable. The repeat size increases across generations (intergenerational instability) and within tissues during a patient's lifetime (somatic instability). The number of inherited repeats and the level of somatic instability correlate with the age of onset and severity of symptoms. Thus, targeting the mutation itself to stabilize or reduce CTG repeat length is the most promising therapeutic strategy, as it would address all the pathophysiological mechanisms resulting from the mutation.Initially, my thesis work focused on identifying repositioned chemical molecules capable of modulating repeat instability. Screening the 1280 molecules from the Prestwick Chemical Library allowed me to identify 39 candidate molecules that alter the expression of a reporter gene, suggesting they could modulate repeat instability. After directly studying their effect on instability, I excluded four of these molecules that do not modulate repeat expression. I demonstrated that a fifth molecule, clomipramine, can modulate repeat instability in the screening cell model but not in murine and human DM1 fibroblasts.Concurrently, I showed that RGFP966, a selective HDAC3 inhibitor, induced contractions of CTG repeats in murine DM1 fibroblasts with approximately 650 repeats. This effect appears to depend on the dose of RGFP966 or the size of the CTG repeat, as it was not replicated in human DM1 fibroblasts with 350 CTG repeats. An RNA-seq approach in murine cells treated with RGFP966 identified several candidate genes involved in DNA replication as possible modifiers of instability. I also showed a decrease in bidirectional DMPK transcription associated with a probable hypermethylation downstream of the repeats in murine DM1 cells. In conclusion, my data suggest that RGFP966 modulates CTG repeat instability in DM1 through multiple mechanisms, potentially including chromatin structure modification at the DM1 locus and alterations in DNA replication.Overall, my thesis project contributed to the understanding of repeat instability mechanisms and the identification of chemical compounds that modulate instability dynamics. My work also highlighted the limitations of each model used and the complexity of identifying small molecules that alter CTG triplet dynamics in reporter cell models. Additionally, I participated in developing long-read sequencing (with and without amplification) for DM1, providing a rapid and highly informative new tool for the analysis of somatic mosaicism
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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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Ubink-Bontekoe, Carola Jacoba Maria. "CGG repeat instability and FXR proteins." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2001. http://hdl.handle.net/1765/12091.

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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 hairpin, coordination between the 5’-flap endonuclease activity of flap endonuclease 1 (FEN1), 3’-5’ exonuclease activity of AP endonuclease 1 (APE1), and activity of DNA ligase I (LIG I) can resolve the double-flap structure produced during BER in the hairpin loop. The resolution of the double-flap structure resulted in hairpin removal and prevention or attenuation of TNR expansions and provides the first evidence that coordination among BER proteins can remove a TNR hairpin. We further explored the role of BER cofactors in modulating TNR instability and found that the repair cofactor proliferating cell nuclear antigen (PCNA) facilitates genomic stability by promoting removal of a TNR hairpin. Hairpin removal was accomplished by altering dynamic TNR structures to allow more efficient FEN1 cleavage and DNA polymerase β (pol β) synthesis and stimulating the activity of LIG I. This study provides the first evidence that a DNA repair cofactor plays an important role in modulating TNR instability. Finally, we explored the effects of sugar modifications in abasic sites on activities of BER proteins and BER efficiency during repair in a TNR tract. We found that an oxidized sugar inhibits the activities of BER enzymes, interrupting their coordination and preventing efficient repair. Inefficient repair results in accumulation of repair intermediates with DNA breaks, contributing to genomic instability. Our results indicate that DNA base lesions and BER play a crucial role in modulating TNR instability. The research presented herein provides a molecular basis for further developing BER as a target for prevention and treatment of neurodegenerative diseases caused by TNR expansion.
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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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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 instability is greater than in wild-type cells but orientation-independent. The observation of single trinucleotide insertions and deletions in these mutator mutants indicates that replication slippages of 3 bp occur <i>in vivo</i> leading to repeat expansion and contraction if left unrepaired. Compared to wild-type cells large deletions are reduced in these mutator mutants, but only if the CTG sequence serves as the lagging strand. Based on the opposing effects of mismatch repair a model is proposed in which orientation-dependent CTG repeat instability in mismatch repair proficient cells is caused by the repair of 3-bp slippages. This leads to the creation of larger deletions during repair synthesis due to the formation of unusual secondary structures by the CTG sequence on the lagging strand. Mutations in the <i>recA</i> and <i>sbcCD </i>genes do not affect the stability of plasmid-borne CTG repeats. Similarly the viability of <i>recA</i>-deficient strains carrying chromosomal insertions of (CTG)<sub>25</sub> and (CTG)<sub>43</sub> suggests that, unlike long palindromes, these trinucleotide repeats are not substrates for the structure-directed nuclease complex SbcCD or, alternatively, they do not form secondary structures frequently enough to cause lethality in <i>recA-</i>deficient hosts. In contrast, a mutation in the <i>recG</i> gene, also involved in homologous recombination, severely destabilises the (CTG)<sub>43</sub> repeat in a strongly orientation-dependent manner that exceeds all other tested mutants. Possible explanations for this observation are discussed.
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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 shorter ones and the orientation where CAG repeats are on the leading strand template is more unstable than the opposite where CTG repeats are on the leading strand template. This orientation-dependence of CAG·CTG trinucleotide repeat instability is determined by the proofreading subunit of DNA polymerase II (DnaQ) in the presence of the hairpin nuclease SbcCD. The analysis of the sizes of deletions observed in wild type and mutant cells is consistent with the formation of secondary structures <i>in vivo</i>. The mismatch repair pathway does not affect the instability of CTG repeats in the <i>E. coli</i> chromosome but influences the CAG orientation. It is suggested that MutS stabilizes CAG repeats by initiating a “repair” process and protecting hairpins from SbcCD, which can cleave hairpins in the presence of MutL and MutH. Finally, the roles of two helicases, Rep and UvrD are analyzed. A mutation in <i>rep</i> helicase strongly destabilizes CTG repeats with no effect on the CAG orientation UvrD mutants show instability in both orientations. The increase in instability in the <i>uvrD</i> mutant depends on RecF in the CTG orientation.
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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 genome resulting in expansion after subsequent cell division. Recent in vitro studies suggested that a family A translesion polymerase, polymerase θ (Polθ), was able to synthesize DNA larger than the template DNA. Clinical and in vivo studies showed either overexpression or knock down of Polθ caused poor survival in breast cancer patients and genomic instability. However, the role of Polθ in TNR expansion remains unelucidated. Therefore, we hypothesize that Polθ can directly cause TNR expansion during DNA synthesis. The investigation of the functional properties of Polθ during DNA replication and TNR synthesis will provide insight for the mechanism of TNR expansion through generations.
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Pickett, Hilda A. "Molecular characterisation of instability in human telomere repeat arrays." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/30343.

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Telomere instability was investigated at the proximal ends of human telomeres in normal and abnormal cells, with the aim to identify the frequency and types of mutations underlying telomere repeat turnover. Analysis of the interspersion patterns of telomere and variant repeat types at the proximal ends of the 12q and Xp/Yp telomeres in human pedigrees gave a germline mutation frequency of 0.6% per telomere per gamete over the proximal 1kb of the telomere repeat array. No somatic telomere mutations were identified in normal fibroblast cells, but the upper limit for the mutation frequency was estimated as 7.468xlO-3 per cell. Each of 7 germline mutation events involved increases or decreases in small numbers of repeats. These events can be explained by intra-allelic mutational mechanisms, such as replication slippage and unequal sister-chromatid exchange. Localised telomere instability was associated with the CTAGGG variant repeat type in 6/7 germline mutations. Approximately 15% of sporadic colon cancers and the majority of tumours from patients with hereditary non polyposis colon cancer (HNPCC) are caused by defects in genes involved in the mismatch repair pathway. Such defects result in an accummulation of mutations, particularly at microsatellite loci. A high mutation frequency was observed in the 12q and Xp/Yp telomere repeat arrays in colon cancers and was particularly associated with tumours showing microsatellite instability. The observed tumour mutations also involved increases or decreases in blocks of like-repeat types and can be explained by intra-allelic mutations. In one tumour, a complex telomere mutation was provisionally identified and may represent an inter-allelic mutation event. No telomeric mutations were observed in the first kilobase of the 12q and Xp/Yp telomeres in cell-lines derived from patients suffering from the premature ageing disorder Werner syndrome. The lack of telomere mutations in Werner syndrome cells is discussed, with respect to overall telomere stability.
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Chan, Nelson Lap Shun. "IDENTIFICATION OF ACTIVITIES INVOLVED IN CAG/CTG REPEAT INSTABILITY." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/832.

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CAG/CTG repeat instability is associated with at least 14 neurological disorders, including Huntington’s disease and Myotonic dystrophy type 1. In vitro and in vivo studies have showed that CAG/CTG repeats form a stable hairpin that is believed to be the intermediate for repeat expansion and contraction. Addition of extra DNA is essential for repeat expansion, so DNA synthesis is one of the keys for repeat expansion. In vivo studies reveal that 3’ CTG slippage with subsequent hairpin formation (henceforth called the 3’ CTG slippage hairpin) occurs during DNA synthesis. It is proposed that hairpin tolerance machinery is activated because prolonged stalling of DNA polymerase triggers severe DNA damage. As a means toward studying the hairpin-mediated expansion, we created a special hairpin substrate, mimicking the 3’ CTG slippage hairpin, to determine which polymerase promotes hairpin bypass. Our studies reveal polymerase β (pol β) is involved in the initial hairpin synthesis while polymerase δ (pol δ) is responsible for the resumption of DNA synthesis beyond the hairpin (extension step). Surprisingly, we also found that the pol δ can remove the short CTG hairpin by excision of the hairpin with its 3’ to 5’ exonuclease activity. Besides repairing the hairpin directly, resolving the hairpin is an alternative pathway to maintain CAG/CTG repeat stability. With limited understanding of which human helicase is responsible for resolving CAG/CTG hairpins, we conducted a screening approach to identify the human helicase involved. Werner Syndrome Protein (WRN) induces the hairpin repair activity when (CTG)35 hairpin is formed on the template strand. Primer extension assay reveals that WRN stimulates pol δ synthesis on (CAG)35/(CTG)35 template and such induction was still found in the presence of accessory factors. Helicase assay confirms that WRN unwinds CTG hairpin structures. Our studies provide a better understanding of how polymerases and helicases play a role in CAG/CTG repeat instability. Considering CAG/CTG repeat instability associated disorders are still incurable, our studies can provide several potential therapeutic targets for treating and/or preventing CAG/CTG repeat associated disorders.
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Books on the topic "Repeat instabilty"

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1946-, Oostra Ben A., ed. Trinucleotide diseases and instability. Springer, 1998.

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Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.

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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.
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Zeitlin, Vladimir. Rotating Shallow-Water model with Horizontal Density and/or Temperature Gradients. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198804338.003.0014.

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The derivation of rotating shallow-water equations by vertical averaging and columnar motion hypothesis is repeated without supposing horizontal homogeneity of density/potential temperature. The so-called thermal rotating shallow-water model arises as the result. The model turns to be equivalent to gas dynamics with a specific equation of state. It is shown that it possesses Hamiltonian structure and can be derived from a variational principle. Its solution at low Rossby numbers should obey the thermo-geostrophic equilibrium, replacing the standard geostrophic equilibrium. The wave spectrum of the model is analysed, and the appearance of a whole new class of vortex instabilities of convective type, resembling asymmetric centrifugal instability and leading to a strong mixing at nonlinear stage, is demonstrated.
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Macartney, Huw. The Bank Culture Debate. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198843764.001.0001.

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Following the global financial crisis and repeated scandals, US and UK state managers made substantial efforts to reform the culture of their banking sectors. This book argues though that they focused on an extremely narrow definition of bank culture. They did so for two reasons: firstly, because the structural pressures of financialization—which are a far more important driver of the problematic features of bank culture in Anglo-America—are harder to remedy; but secondly, state managers also used their bank culture response to tackle a legitimacy crisis facing their institutions of government. In so doing they abdicated responsibility for the real problems—of inequality and instability—associated with their respective financial systems. Drawing on interviews with over 150 bankers this book explains the strategies employed by state managers before then examining what has and has not changed in the culture of banking in the US and UK.
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The Global State of Democracy 2022: Forging Social Contracts in a Time of Discontent. International Institute for Democracy and Electoral Assistance (International IDEA), 2022. http://dx.doi.org/10.31752/idea.2022.56.

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At the end of 2022, the world is trapped beneath the weight of a multitude of old and new problems. There are myriad causes of political and economic instability, including the spiking prices of food and energy, ballooning inflation and an impending recession. These phenomena are occurring in the unstable context of continuing climate change, long unresolved inequality, the Covid-19 pandemic, declining standards of living and the Russian war of aggression in Ukraine. Democratic institutions are especially important in times of crisis and fear. They ensure open pathways for the information and communication that citizens and governments need to be able to act responsively and effectively. To rebuild and revitalize these institutions and to re-establish trust between the people and their governments, it is necessary to develop new and innovative social contracts that better reflect the changing global environment and that meaningfully prioritize equal access to the mechanisms of participation. International IDEA’s Global State of Democracy Report 2022 provides an overview of the global and regional trends related to democracy and human rights, along with examples of efforts to reinvigorate social contracts around the world.
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Hanning, Robert W. Boccaccio, Chaucer, and Stories for an Uncertain World. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780192894755.001.0001.

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The fictive inhabitants of the Decameron and the Canterbury Tales, the stories they tell each other, and the framing fictions that bring them together collectively acknowledge a radical uncertainty that characterizes most human endeavors, challenging the achievement of effective knowledge, perception, and strategy, and lacking intervention by Divine Providence. Dependable knowledge of the future, the past, or the distant present is thwarted by the fickle forces of chance (fortuna) and unverifiable report (fama); accurate perception of meaning is compromised by the instability or equivocality of all systems of signification, linguistic or symbolic, and by the notorious opacity of human intention; and successful strategies for dealing with power in its many forms founder on power’s chronic arbitrariness and irrationality. The key to coping with these challenges is pragmatic prudence: rational calculation issuing in an opportunistic, often amoral choice of ingenious deeds and/or eloquent words appropriate (though without guarantee) to mastering a specific crisis. The goal of pragmatic prudence is agency now, not salvation later. Following an initial chapter that explores the Aristotelian antecedents, contemporaneous cultural influences, and narrative techniques shaping the radically uncertain world of the Decameron and the Canterbury Tales, and identifies components of pragmatic prudence animating the quest for agency in both collections, succeeding chapters pair, and compare, novelle and pilgrim tales that illustrate that quest—its successes and its failures—as it confronts the challenges posed by chance, faulty communication, the unstable referentiality of signifying systems, hidden intentions, and both institutional and emotional power.
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Book chapters on the topic "Repeat instabilty"

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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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Parniewski, Pawel, and Pawel Staczek. "Molecular Mechanisms of TRS Instability." In Triple Repeat Diseases of the Nervous Systems. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0117-6_1.

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Curtis, J. Willard. "Churning: Repeated Optimization and Cooperative Instability." In Cooperative Systems. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4613-0219-3_6.

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Salina, E. A., E. G. Pestsova, and N. P. Goncharov. "Instability of Subtelomeric Spelt1 Repeats of Wheat Species." In Stadler Genetics Symposia Series. Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4235-3_23.

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Polleys, Erica J., and Catherine H. Freudenreich. "Methods to Study Repeat Fragility and Instability in Saccharomyces cerevisiae." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7306-4_28.

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Walker, Catherine A., and Catherine M. Abbott. "Trinucleotide Repeat Instability as a Cause of Human Genetic Disease." In Encyclopedia of Genetics. Routledge, 2014. http://dx.doi.org/10.4324/9781315073972-55.

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Mowbray, Miranda. "Observable Instability for the Repeated Prisoner’s Dilemma." In Approximation, Optimization and Mathematical Economics. Physica-Verlag HD, 2001. http://dx.doi.org/10.1007/978-3-642-57592-1_20.

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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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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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Kobayashi, Takehiko. "Genome Instability of Repetitive Sequence: Lesson from the Ribosomal RNA Gene Repeat." In DNA Replication, Recombination, and Repair. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55873-6_10.

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Conference papers on the topic "Repeat instabilty"

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Akatsuka, T., H. Imai, K. Arai, et al. "Highly stable laser repeater system with frequency instability below 10-21." In Conference on Lasers and Electro-Optics/Pacific Rim. Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleopr.2022.cfa6g_02.

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We report an ultralow-noise laser repeater system based on a narrow-linewidth laser and a planar lightwave circuit chip. An out-of-loop measurement demonstrates a record frequency instability of 3 × 10-22 at 30,000 s averaging time.
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Grasser, Tibor. "Towards Understanding Negative Bias Temperature Instability." In 2008 IEEE International Integrated Reliability Workshop Final Report (IRW). IEEE, 2008. http://dx.doi.org/10.1109/irws.2008.4796147.

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Grasser, Tibor. "Towards Understanding Negative Bias Temperature Instability." In 2008 IEEE International Integrated Reliability Workshop Final Report (IRW). IEEE, 2008. http://dx.doi.org/10.1109/irws.2008.4796110.

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Hensman Moss, Davina, Anupriya Dalmia, Valentina Galassi Deforie, et al. "C12 HTT repeat instability in family trios in the 100,000 genomes project." In EHDN 2022 Plenary Meeting, Bologna, Italy, Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jnnp-2022-ehdn.56.

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Zafar, Sufi. "The Negative Bias Temperature Instability in MOS Devices." In 2006 IEEE International Integrated Reliability Workshop Final Report. IEEE, 2006. http://dx.doi.org/10.1109/irws.2006.305255.

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Hongyu Zhao, Yue Zhao, Rong Chai, and Lu Cai. "Instability of the DNA repeats mutation in humans hereditary disorders." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5965950.

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Lelis, A. J., R. Green, D. Habersat, and N. Goldsman. "Effect of Threshold-Voltage Instability on SiC DMOSFET Reliability." In 2008 IEEE International Integrated Reliability Workshop Final Report (IRW). IEEE, 2008. http://dx.doi.org/10.1109/irws.2008.4796090.

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Lelis, Aivars, D. Habersat, R. Green, and N. Goldsman. "Effect of Threshold-Voltage Instability on SiC DMOSFET Reliability." In 2008 IEEE International Integrated Reliability Workshop Final Report (IRW). IEEE, 2008. http://dx.doi.org/10.1109/irws.2008.4796136.

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Lelis, A. J., S. Potbhare, D. Habersat, G. Pennington, and N. Goldsman. "Modeling and Characterization of Bias Stress-Induced Instability of SiC MOSFETs." In 2006 IEEE International Integrated Reliability Workshop Final Report. IEEE, 2006. http://dx.doi.org/10.1109/irws.2006.305235.

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Grasser, Tibor, Paul-Jurgen Wagner, Philipp Hehenberger, Wolfgang Gos, and Ben Kaczer. "A rigorous study of measurement techniques for negative bias temperature instability." In 2007 IEEE International Integrated Reliability Workshop Final Report. IEEE, 2007. http://dx.doi.org/10.1109/irws.2007.4469212.

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Reports on the topic "Repeat instabilty"

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Brunner, Huschenbett, and Beshouri. PR-336-06206-R01 Engine Control for Legacy Engines - Cylinder and Cycle Level Control. Pipeline Research Council International, Inc. (PRCI), 2014. http://dx.doi.org/10.55274/r0010041.

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The reduction or even elimination of cylinder to cylinder combustion variation and cycle-to-cycle combustion instability may result in further nitrous oxides (NOx) reductions at the same engine average air/fuel ratio (and hence turbocharger operating point) or allow operation at a leaner air/fuel ratio before the onset of instability. Reductions in imbalance and instability can also reduce carbon pollutant emissions, reduce break specific fuel consumption (BSFC) and improve engine operability. Achieving these goals requires a better understanding of the sources and impacts of that imbalance and instability and then the development techniques to reduce if not eliminate both. This effort focuses on combustion instability of legacy large bore pipeline reciprocating engines operating at very high air/fuel ratios to meet higher emission standards. The report provides a detailed cycle-to-cycle analysis of acquired pressure and ion current data of four test engines in-cluding Clark T-series family and Cooper Bessemer GMV/W engines. The possibility of upcom-ing misfire or poor combustion prediction is investigated and discussed. The document further investigates advanced cylinder balancing strategies as well as the benefits of improved pre-combustion chamber performance.
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Chao, Alex. Very Large Hadron Collider Instability Workshop Summary Report. Office of Scientific and Technical Information (OSTI), 2001. http://dx.doi.org/10.2172/784899.

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Lahey, R. T. Jr. Analysis of nuclear reactor instability phenomena. Progress report. Office of Scientific and Technical Information (OSTI), 1993. http://dx.doi.org/10.2172/10131526.

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Aluie, Hussein. Final Technical Report: Ablative Magnetohydrodynamic Rayleigh-Taylor Instability. Office of Scientific and Technical Information (OSTI), 2023. http://dx.doi.org/10.2172/2311793.

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Ismail, Zenobia. Interaction Between Food Prices and Political Instability. Institute of Development Studies (IDS), 2021. http://dx.doi.org/10.19088/k4d.2021.091.

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This report reviews the literature on links between international food prices and political instability (including protests, riots and social unrest). The literature on food prices and protests, riots, unrest, or violent incidents consists mainly of peer-reviewed scholarly articles that utilise econometric modeling. Some early studies examined the links between international food prices and political instability and found conflicting results. Some assessments concluded that there were links between international food prices or food insecurity and the number of violent incidents, while others found that such a link was tenuous. This literature review covers some of the main arguments and findings in the recent literature on food prices and political instability or conflict. The majority of the econometric studies in this review find that there is a link between food price increases and a greater probability of protests, riots or social unrest. However, there are still a few studies that have contradictory results. So, the debate on the effect of food prices on political stability continues. Food subsidies, cash transfers, price controls, and the elimination of trade barriers are some of the policy interventions that may address rising food prices and mitigate the rise of violent collective action. However, the literature questions the effectiveness of such policies in cases where violence or protest action stems from deeper, underlying economic or political grievances.
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Dynan, William S. Final Technical Report - Mechanisms and pathways controlling genomic instability. Office of Scientific and Technical Information (OSTI), 2013. http://dx.doi.org/10.2172/1081424.

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Dynan, William S. Final report- Links between persistent DNA damage, genome instability, and aging. Office of Scientific and Technical Information (OSTI), 2016. http://dx.doi.org/10.2172/1333814.

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Majda, Andrew J. Report: Low Frequency Predictive Skill Despite Structural Instability and Model Error. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada601429.

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Mizuno, K., J. S. DeGroot, R. P. Drake, and W. Seka. Collective Thomson scattering measurements of the Ion Acoustic Decay Instability. Final report. Office of Scientific and Technical Information (OSTI), 1993. http://dx.doi.org/10.2172/10143761.

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Young, P., P. Drake, Estabrook, K. Mizuno, and J. S. De Groot. Final report of investigation of the Acoustic Decay Instability in laser plasma interaction. Office of Scientific and Technical Information (OSTI), 1991. http://dx.doi.org/10.2172/6027882.

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