Chromatin remodelling and DNA replication: from nucleosomes to loop domains

Demeret, Caroline; Vassetzky, Yegor S.; Méchali, Marcel

doi:10.1038/sj.onc.1204333

Cited by 59 publications

(34 citation statements)

References 98 publications

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“…Chromosomal domains (loop domains) are the basic structural and topological units in eukaryotic chromatin and have been detected in many organisms, including humans (92)(93)(94)(95)(96)(97)(98). These loops range in size from 5 to 200 kbp with an average size of 80 -100 kbp for somatic cells and ϳ30 kbp for male gametes (92)(93)(94)99).…”

Section: Discussionmentioning

confidence: 99%

Increased Negative Superhelical Density in Vivo Enhances the Genetic Instability of Triplet Repeat Sequences

Напиерала

Bacolla

Wells

2005

Journal of Biological Chemistry

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The influence of negative superhelical density on the genetic instabilities of long GAA⅐TTC, CGG⅐CCG, and CTG⅐CAG repeat sequences was studied in vivo in topologically constrained plasmids in Escherichia coli. These repeat tracts are involved in the etiologies of Friedreich ataxia, fragile X syndrome, and myotonic dystrophy type 1, respectively. The capacity of these DNA tracts to undergo deletions-expansions was explored with three genetic-biochemical approaches including first, the utilization of topoisomerase I and/or DNA gyrase mutants, second, the specific inhibition of DNA gyrase by novobiocin, and third, the genetic removal of the HU protein, thus lowering the negative supercoil density (؊). All three strategies revealed that higher ؊ in vivo enhanced the formation of deleted repeat sequences. The effects were most pronounced for the Friedreich ataxia and the fragile X triplet repeat sequences. Higher levels of ؊ stabilize non-B DNA conformations (i.e. triplexes, sticky DNA, flexible and writhed DNA, slipped structures) at appropriate repeat tracts; also, numerous prior genetic instability investigations invoke a role for these structures in promoting the slippage of the DNA complementary strands. Thus, we propose that the in vivo modulation of the DNA structure, localized to the repeat tracts, is responsible for these behaviors. Presuming that these interrelationships are also found in humans, dynamic alterations in the chromosomal nuclear matrix may modulate the ؊ of certain DNA regions and, thus, stabilize/destabilize certain non-B conformations which regulate the genetic expansions-deletions responsible for the diseases.Genetic instability of microsatellite sequences have been widely observed throughout genomes of all organisms studied (1-3). In the majority of cases this phenomenon occurs without phenotypical consequences, but in some circumstances instability (mostly expansions of the repeat tracts) results in the development of disease (1, 4, 5). Expansions of tri-, tetra-and pentanucleotide microsatellites are related to the etiology of more than 20 neurological diseases including myotonic dystrophy types I and II, fragile X syndrome, Friedreich ataxia, and spinocerebellar ataxias (1,4,5).Studies on the mechanisms of trinucleotide repeat sequence (TRS) 2 expansions have revealed that replication, recombination, and repair, probably acting in concert, are responsible for the instabilities of the repetitive tracts (1, 4 -7). Several cis elements as well as trans-acting factors influencing genetic instabilities were discovered (8 -11). The sequences of the repeats, their length, and the presence of polymorphisms (interruptions) in the repeating tract are among the most important determinants of the extent of their instability (10,(12)(13)(14)(15). In addition, the orientation of the repeats relative to the origin of replication, their distance from the origin, transcription through the repeats, and DNA methylation status are factors (9, 16 -21).Expansions of the repeats in affected individuals occur ...

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Section: Discussionmentioning

confidence: 99%

Increased Negative Superhelical Density in Vivo Enhances the Genetic Instability of Triplet Repeat Sequences

Напиерала

Bacolla

Wells

2005

Journal of Biological Chemistry

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“…Nucleosomes and transcription complexes are disrupted by replication fork progression (Sogo et al, 1986;Wol e and Brown, 1986). The ensuing competition provides a window of opportunity for the reprogramming of states of gene activity (Demeret et al, 2001;Barton and Crowe, 2001). …”

Section: Chromatin Remodeling Machinesmentioning

confidence: 99%

Chromatin remodeling: why it is important in cancer

Wolffe

2001

Oncogene

101

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“…Previous studies have confirmed that the change in the timing of DNA replication involves epigenetic regulations, such as methylamination (Parada and Misteli, 2002;Ensminger and Chess, 2004), phosphorylation (Smith et al, 2001), or deacetylation (Demeret et al, 2001).…”

Section: Discussionmentioning

confidence: 98%

“…They considered the possible reason for this effect to be the deletion and/or rearrangement of one arm of the affected chromosome, leading to the deletion or mutation of a cis element that normally establishes early replication timing, resulting in delayed replication of the entire chromosome. Demeret et al (2001) also reviewed chromatin remodeling complexes featuring histone deacetylase activity, and found that such complexes may be involved in DNA replication by embedding origins of replication into a repressive, deacetylated chromatin structure, which would reduce their accessibility to replication factors, delaying the timing of DNA duplication during the S phase, as observed for heterochromatin.…”

Section: Discussionmentioning

confidence: 99%

Replication timing regulation in adults with chromosomal balance rearrangements

Xie¹,

Wu²,

Su³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The alternative forms of the alleles in biallelic genes display a synchronous pattern of replication that is different from genes subjected to monoallelic expression, which exhibit an asynchronous mode of replication. The present study sought to gain insight into changes in the allele-specific replication timing in phenotypically normal humans with balanced chromosomal rearrangements, and to investigate the potential mechanism for chromosomal rearrangements. We used fluorescence in situ hybridization and chose biallelic gene expression of RB1 and monoallelic expression of SNRPN in phytohemagglutininstimulated lymphocytes to compare differences in the allelic replication timing. We found that compared to genetically normal adult controls, adults with a normal phenotype despite chromosomal rearrangements showed normal replication timing (synchronous or asynchronous) for the RB1 gene and SNRPN genes. Our data support a link between chromosomal aberrations and epigenetic stability in phenotypically normal humans, independent of the breakpoints in chromosomal structural disruption, and represent an epigenetic mark for allelic exclusion in balanced chromosomal rearrangements in patients with normal phenotypes.

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Chromatin remodelling and DNA replication: from nucleosomes to loop domains

Cited by 59 publications

References 98 publications

Increased Negative Superhelical Density in Vivo Enhances the Genetic Instability of Triplet Repeat Sequences

Increased Negative Superhelical Density in Vivo Enhances the Genetic Instability of Triplet Repeat Sequences

Chromatin remodeling: why it is important in cancer

Replication timing regulation in adults with chromosomal balance rearrangements

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