ArticleNucleic acids research2011
Role of transcript and interplay between transcription and replication in triplet-repeat instability in mammalian cells.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Triplex H-DNA structure: the long and winding road from the discovery to its role in human disease.NAR molecular medicine · 2024Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- R-loops: targets for nuclease cleavage and repeat instability.Current genetics · 2018Review
- RNA-DNA hybrids promote the expansion of Friedreich's ataxia (GAA)n repeats via break-induced replication.Nucleic acids research · 2018Article
- The effects of transcription and recombination on mutational dynamics of short tandem repeats.Nucleic acids research · 2018Article
- Friedreich's ataxia-associated GAA repeats induce replication-fork reversal and unusual molecular junctions.Nature structural & molecular biology · 2013Article
- Genome-wide screen identifies pathways that govern GAA/TTC repeat fragility and expansions in dividing and nondividing yeast cells.Molecular cell · 2012Article
- Role of mismatch repair enzymes in GAA·TTC triplet-repeat expansion in Friedreich ataxia induced pluripotent stem cells.The Journal of biological chemistry · 2012Article
- Transcription as a source of genome instability.Nature reviews. Genetics · 2012Review
- Article
- Stabilization of expanded (CTG)•(CAG) repeats by antisense oligonucleotides.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- DNA dynamics is likely to be a factor in the genomic nucleotide repeats expansions related to diseases.PloS one · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Triplet-repeat expansions cause several inherited human diseases. Expanded triplet-repeats are unstable in somatic cells, and tissue-specific somatic instability contributes to disease pathogenesis. In mammalian cells instability of triplet-repeats is dependent on the location of the origin of replication relative to the repeat tract, supporting the 'fork-shift' model of repeat instability. Disease-causing triplet-repeats are transcribed, but how this influences instability remains unclear. We examined instability of the expanded (GAA•TTC)(n) sequence in mammalian cells by analyzing individual replication events directed by the SV40 origin from five different locations, in the presence and absence of doxycycline-induced transcription. Depending on the location of the SV40 origin, either no instability was observed, instability was caused by replication with no further increase due to transcription, or instability required transcription. Whereas contractions accounted for most of the observed instability, one construct showed expansions upon induction of transcription. These expansions disappeared when transcript stability was reduced via removal or mutation of a spliceable intron. These results reveal a complex interrelationship of transcription and replication in the etiology of repeat instability. While both processes may not be sufficient for the initiation of instability, transcription and/or transcript stability seem to further modulate the fork-shift model of triplet-repeat instability.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.