Pausing of simian virus 40 DNA replication fork movement in vivo by (dG-dA)n·(dT-dC)n tracts

Rao, B. Sanjiva

doi:10.1016/0378-1119(94)90549-5

Cited by 36 publications

(23 citation statements)

References 20 publications

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“…An H-DNA-forming sequence GA (20) in the simian virus 40 (SV40) genome slowed growth in monkey CV1 cells, resulting in lower titers and smaller plaques [133]. GA repeats reduced the rate of nucleotide incorporation into the SV40 genome, resulting in stalled replication forks [133,134]. E. coli strains transformed with plasmids containing the 2.5-kbp polypyrimidine sequence from the human PKD1 gene grew slower than those had shorter inserts, and this effect correlated with the level of negative supercoiling of the plasmid DNA in vivo, suggesting that the H-DNA structures formed were responsible for the cell growth retardation [135].…”

Section: Influences Of H-dna On Dna Replication and Repairmentioning

confidence: 99%

DNA triple helices: Biological consequences and therapeutic potential

Jain

Wang²,

Vásquez³

2008

Biochimie

259

199

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DNA structure is a critical element in determining its function. The DNA molecule is capable of adopting a variety of non-canonical structures, including three-stranded (i.e. triplex) structures, which will be the focus of this review. The ability to selectively modulate the activity of genes is a longstanding goal in molecular medicine. DNA triplex structures, either intermolecular triplexes formed by binding of an exogenously applied oligonucleotide to a target duplex sequence, or naturally occurring intramolecular triplexes (H-DNA) formed at endogenous mirror repeat sequences, present exploitable features that permit site-specific alteration of the genome. These structures can induce transcriptional repression and site-specific mutagenesis or recombination. Triplex-forming oligonucleotides (TFOs) can bind to duplex DNA in a sequence specific fashion with high affinity, and can be used to direct DNA-modifying agents to selected sequences. H-DNA plays important roles in vivo and is inherently mutagenic and recombinogenic, such that elements of the H-DNA structure may be pharmacologically exploitable. In this review we discuss the biological consequences and therapeutic potential of triple helical DNA structures. We anticipate that the information provided will stimulate further investigations aimed toward improving DNA triplexrelated gene targeting strategies for biotechnological and potential clinical applications.

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Section: Influences Of H-dna On Dna Replication and Repairmentioning

confidence: 99%

DNA triple helices: Biological consequences and therapeutic potential

Jain

Wang²,

Vásquez³

2008

Biochimie

259

199

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“…Preferential deletion of repeats on the lagging strand was observed, supporting the formation of these structures on the lagging-strand template (282). In vivo, replication inhibition due to the formation of unusual DNA structures was first proposed for the (GA) n /(TC) n repeat (244,245) and the GA-rich repeat from the hamster dhfr gene (23) in mammalian cells. Later on, this issue was mostly studied for trinucleotide repeats that are involved in a variety of expansion diseases (see below).…”

Section: Unusual Dna Structuresmentioning

confidence: 84%

Replication Fork Stalling at Natural Impediments

Mirkin

2007

Microbiol Mol Biol Rev

452

466

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SUMMARY Accurate and complete replication of the genome in every cell division is a prerequisite of genomic stability. Thus, both prokaryotic and eukaryotic replication forks are extremely precise and robust molecular machines that have evolved to be up to the task. However, it has recently become clear that the replication fork is more of a hurdler than a runner: it must overcome various obstacles present on its way. Such obstacles can be called natural impediments to DNA replication, as opposed to external and genetic factors. Natural impediments to DNA replication are particular DNA binding proteins, unusual secondary structures in DNA, and transcription complexes that occasionally (in eukaryotes) or constantly (in prokaryotes) operate on replicating templates. This review describes the mechanisms and consequences of replication stalling at various natural impediments, with an emphasis on the role of replication stalling in genomic instability.

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“…7b, but much longer although imperfect tracts of more than 50 nt are also present in this region. Polypurine/ polypyrimidine tracts can potentially form non-B-form structure such as triplex DNA, which is known to arrest the replication fork movement in vitro (2,8,14,45). Although these functions have not been confirmed in vivo, the sequences with biased composition found in the switch region may play roles in regulating DNA replication fork movement (see Discussion).…”

Section: Resultsmentioning

confidence: 99%

“…The identified switch region has some characteristic sequences, which we assume to be candidates for causing the termination (or pausing) of replication fork movement. One is a polypurine/polypyrimidine tract, some of which are known to arrest the replication fork movement in vitro (2,8,14,45), although the function in vivo has been scarcely examined. The other candidate is an SAR.…”

Section: Figmentioning

confidence: 99%

Precise Switching of DNA Replication Timing in the GC Content Transition Area in the Human Major Histocompatibility Complex

Tenzen

Yamagata

Fukagawa

et al. 1997

Molecular and Cellular Biology

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The human genome is composed of long-range G؉C% (GC%) mosaic structures thought to be related to chromosome bands. We previously reported a boundary of megabase-sized GC% mosaic domains at the junction area between major histocompatibility complex (MHC) classes II and III, proposing it as a possible chromosome band boundary. DNA replication timing during the S phase is known to be correlated cytogenetically with chromosome band zones, and thus the band boundaries have been predicted to contain a switch point for DNA replication timing. In this study, to identify to the nucleotide sequence level the replication switch point during the S phase, we determined the precise DNA replication timing for MHC classes II and III, focusing on the junction area. To do this, we used PCR-based quantitation of nascent DNA obtained from synchronized human myeloid leukemia HL60 cells. The replication timing changed precisely in the boundary region with a 2-h difference between the two sides, supporting the prediction that this region may be a chromosome band boundary. We supposed that replication fork movement terminates (pauses) or significantly slows in the switch region, which contains dense Alu clusters; polypurine/polypyrimidine tracts; di-, tri-, or tetranucleotide repeats; and medium-reiteration-frequency sequences. Because the nascent DNA in the switch region was recovered at low efficiency, we investigated whether this region is associated with the nuclear scaffold and found three scaffold-associated regions in and around the switch region.The genomes of warm-blooded vertebrates, including humans, are composed of large-scale compartmentalized structures, one of which consists of long-range GϩC% (GC%) mosaic structures. The mosaics of long-range regions (Ͼ300 kb) homogeneous in GC% are called isochores by Bernardi et al. (5). Several groups, including ours, showed that the GC% mosaic structures are related to chromosome bands (1,5,23,28,29,31,44). Giemsa-dark G bands are composed mainly of AT-rich sequences, whereas T bands (a subgroup of Giemsapale R bands) are composed mainly of GC-rich sequences: ordinary R bands are heterogeneous and appear to be intermediate in GϩC content (3,4,12,(32)(33)(34)47). Another aspect of genome compartmentalization is the replication time zone. Mammalian DNA replication timing is roughly divided into early S (S E ) and late S (S L ) phases (16, 25, 38); G-band zones replicate primarily during S L , whereas R-band zones, including T bands, replicate in S E (27). Therefore, band boundaries have been presumed to be precisely assignable at the nucleotide sequence level by identifying the early-to-late switch point for replication timing. We would predict that this region is where regulatory signals for DNA replication exist. Band boundaries should also be suitable for studying the mechanisms involved in termination, pausing, and/or slowing of DNA replication fork movement.The human major histocompatibility complex (MHC) is known at a high-resolution level to be composed of plural bands (49, 53...

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Pausing of simian virus 40 DNA replication fork movement in vivo by (dG-dA)n·(dT-dC)n tracts

Cited by 36 publications

References 20 publications

DNA triple helices: Biological consequences and therapeutic potential

DNA triple helices: Biological consequences and therapeutic potential

Replication Fork Stalling at Natural Impediments

Precise Switching of DNA Replication Timing in the GC Content Transition Area in the Human Major Histocompatibility Complex

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