Academic literature on the topic 'Strand-slippage replication'

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Journal articles on the topic "Strand-slippage replication"

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Guo, Pei, and Sik Lok Lam. "Unusual structures of CCTG repeats and their participation in repeat expansion." Biomolecular Concepts 7, no. 5-6 (2016): 331–40. http://dx.doi.org/10.1515/bmc-2016-0024.

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AbstractCCTG repeat expansion in intron 1 of the cellular nucleic acid-binding protein (CNBP) gene has been identified to be the genetic cause of myotonic dystrophy type 2 (DM2). Yet the underlying reasons for the genetic instability in CCTG repeats remain elusive. In recent years, CCTG repeats have been found to form various types of unusual secondary structures including mini-dumbbell (MDB), hairpin and dumbbell, revealing that there is a high structural diversity in CCTG repeats intrinsically. Upon strand slippage, the formation of unusual structures in the nascent strand during DNA replica
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Erdeniz, Naz, Sandra Dudley, Regan Gealy, Sue Jinks-Robertson, and R. Michael Liskay. "Novel PMS1 Alleles Preferentially Affect the Repair of Primer Strand Loops during DNA Replication." Molecular and Cellular Biology 25, no. 21 (2005): 9221–31. http://dx.doi.org/10.1128/mcb.25.21.9221-9231.2005.

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ABSTRACT Null mutations in DNA mismatch repair (MMR) genes elevate both base substitutions and insertions/deletions in simple sequence repeats. Data suggest that during replication of simple repeat sequences, polymerase slippage can generate single-strand loops on either the primer or template strand that are subsequently processed by the MMR machinery to prevent insertions and deletions, respectively. In the budding yeast Saccharomyces cerevisiae and mammalian cells, MMR appears to be more efficient at repairing mispairs comprised of loops on the template strand compared to loops on the prime
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Denkiewicz-Kruk, Milena, Malgorzata Jedrychowska, Shizuko Endo та ін. "Recombination and Pol ζ Rescue Defective DNA Replication upon Impaired CMG Helicase—Pol ε Interaction". International Journal of Molecular Sciences 21, № 24 (2020): 9484. http://dx.doi.org/10.3390/ijms21249484.

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The CMG complex (Cdc45, Mcm2–7, GINS (Psf1, 2, 3, and Sld5)) is crucial for both DNA replication initiation and fork progression. The CMG helicase interaction with the leading strand DNA polymerase epsilon (Pol ε) is essential for the preferential loading of Pol ε onto the leading strand, the stimulation of the polymerase, and the modulation of helicase activity. Here, we analyze the consequences of impaired interaction between Pol ε and GINS in Saccharomyces cerevisiae cells with the psf1-100 mutation. This significantly affects DNA replication activity measured in vitro, while in vivo, the p
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Canceill, Danielle, Enrique Viguera, and S. Dusko Ehrlich. "Replication Slippage of Different DNA Polymerases Is Inversely Related to Their Strand Displacement Efficiency." Journal of Biological Chemistry 274, no. 39 (1999): 27481–90. http://dx.doi.org/10.1074/jbc.274.39.27481.

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Tran, H. T., N. P. Degtyareva, N. N. Koloteva, et al. "Replication slippage between distant short repeats in Saccharomyces cerevisiae depends on the direction of replication and the RAD50 and RAD52 genes." Molecular and Cellular Biology 15, no. 10 (1995): 5607–17. http://dx.doi.org/10.1128/mcb.15.10.5607.

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Small direct repeats, which are frequent in all genomes, are a potential source of genome instability. To study the occurrence and genetic control of repeat-associated deletions, we developed a system in the yeast Saccharomyces cerevisiae that was based on small direct repeats separated by either random sequences or inverted repeats. Deletions were examined in the LYS2 gene, using a set of 31- to 156-bp inserts that included inserts with no apparent potential for secondary structure as well as two quasipalindromes. All inserts were flanked by 6- to 9-bp direct repeats of LYS2 sequence, providi
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MacLean, Helen E., Jenny M. Favaloro, Garry L. Warne, and Jeffrey D. Zajac. "Double-strand DNA break repair with replication slippage on two strands: a novel mechanism of deletion formation." Human Mutation 27, no. 5 (2006): 483–89. http://dx.doi.org/10.1002/humu.20327.

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Galli, Alvaro, and Robert H. Schiestl. "Effects of DNA Double-Strand and Single-Strand Breaks on Intrachromosomal Recombination Events in Cell-Cycle-Arrested Yeast Cells." Genetics 149, no. 3 (1998): 1235–50. http://dx.doi.org/10.1093/genetics/149.3.1235.

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Abstract Intrachromosomal recombination between repeated elements can result in deletion (DEL recombination) events. We investigated the inducibility of such intrachromosomal recombination events at different stages of the cell cycle and the nature of the primary DNA lesions capable of initiating these events. Two genetic systems were constructed in Saccharomyces cerevisiae that select for DEL recombination events between duplicated alleles of CDC28 and TUB2. We determined effects of double-strand breaks (DSBs) and single-strand breaks (SSBs) between the duplicated alleles on DEL recombination
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Adams, A. K., and C. Holm. "Specific DNA replication mutations affect telomere length in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 9 (1996): 4614–20. http://dx.doi.org/10.1128/mcb.16.9.4614.

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To investigate the relationship between the DNA replication apparatus and the control of telomere length, we examined the effects of several DNA replication mutations on telomere length in Saccharomyces cerevisiae. We report that a mutation in the structural gene for the large subunit of DNA replication factor C (cdc44/rfc1) causes striking increases in telomere length. A similar effect is seen with mutations in only one other DNA replication gene: the structural gene for DNA polymerase alpha (cdc17/pol1) (M.J. Carson and L. Hartwell, Cell 42:249-257, 1985). For both genes, the telomere elonga
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Freudenreich, C. H., J. B. Stavenhagen, and V. A. Zakian. "Stability of a CTG/CAG trinucleotide repeat in yeast is dependent on its orientation in the genome." Molecular and Cellular Biology 17, no. 4 (1997): 2090–98. http://dx.doi.org/10.1128/mcb.17.4.2090.

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Trinucleotide repeat expansion is the causative mutation for a growing number of diseases including myotonic dystrophy, Huntington's disease, and fragile X syndrome. A (CTG/CAG)130 tract cloned from a myotonic dystrophy patient was inserted in both orientations into the genome of Saccharomyces cerevisiae. This insertion was made either very close to the 5' end or very close to the 3' end of a URA3 transcription unit. Regardless of its orientation, no evidence was found for triplet-mediated transcriptional repression of the nearby gene. However, the stability of the tract correlated with its or
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Petojevic, Tatjana, James J. Pesavento, Alessandro Costa, et al. "Cdc45 (cell division cycle protein 45) guards the gate of the Eukaryote Replisome helicase stabilizing leading strand engagement." Proceedings of the National Academy of Sciences 112, no. 3 (2015): E249—E258. http://dx.doi.org/10.1073/pnas.1422003112.

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DNA replication licensing is now understood to be the pathway that leads to the assembly of double hexamers of minichromosome maintenance (Mcm2–7) at origin sites. Cell division control protein 45 (Cdc45) and GINS proteins activate the latent Mcm2–7 helicase by inducing allosteric changes through binding, forming a Cdc45/Mcm2-7/GINS (CMG) complex that is competent to unwind duplex DNA. The CMG has an active gate between subunits Mcm2 and Mcm5 that opens and closes in response to nucleotide binding. The consequences of inappropriate Mcm2/5 gate actuation and the role of a side channel formed be
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Dissertations / Theses on the topic "Strand-slippage replication"

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"NMR investigations of strand slippage in CTG repeat expansion and primer-template misalignment in low fidelity DNA replication." Thesis, 2007. http://library.cuhk.edu.hk/record=b6074435.

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CTG repeat is one of the most common triplet repeat sequences that have been found to form slipped-strand structures leading to self-expansion during DNA replication. The lengthening of these repeats causes the onset of neurodegenerative diseases such as myotonic dystrophy. Through designing a series of CTG repeat sequences with high hairpin populations, systematic analysis of imino and methyl proton spectra study has been carried out to investigate the length and structural roles of CTG repeats in affecting the propensity of hairpin formation. Direct NMR evidence has been obtained to support
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