DNA–topoisomer analysis on the basis of the helical wormlike chain

Shimada, Jiro; Yamakawa, Hiromi

doi:10.1002/bip.360230503

Cited by 19 publications

(11 citation statements)

References 14 publications

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“…n = 0.5. We obtain for this n { ( Wr) 2 } = (0.8±0.3) 10-3 , whereas on the basis of data from (20,21) one can arrive at the figure of 1.0·10-3 • Thus, for very small as well as for large n our present calculations agree with available theoretical data.…”

Section: Frank-kamenetskii Eta/supporting

confidence: 84%

“…Let us compare our data with the results of Shimada and Yamakawa (20,21). Since their analysis presupposes that n = L!2a is small, such a comparison is sensible only …”

Section: Resultsmentioning

confidence: 80%

“…Shimada and Yamakawa (20,21) were the first to treat theoretically the problem of distribution of wormlike polymer rings over the writhing number. However, since they expressed the distribution function as a power series in L/2a their results may be applied only to very small DNA rings for which the writhing contribution to the ((ALk) 2 } value is virtually negligible.…”

Section: Theorymentioning

confidence: 99%

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Torsional and Bending Rigidity of the Double Helix from Data on Small DNA Rings

Frank‐Kamenetskii

Lukashin

Anshelevich

et al. 1985

Journal of Biomolecular Structure and Dynamics

127

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We have calculated the variance of equilibrium distribution of a circular wormlike polymer chain over the writhing number, [Wr)2), as a function of the number of Kuhn statistical segments, n. For large n these data splice well with our earlier results obtained for a circular freely jointed polymer chain. Assuming that [delta Lk)2) = [delta Tw)2) we have compared our results with experimental data on the chain length dependence of the [delta Lk)2) value recently obtained by Horowitz and Wang for small DNA rings. This comparison has shown an excellent agreement between theory and experiment and yielded a reliable estimate of the torsional and bending rigidity parameters. Namely, the torsional rigidity constant is C = 3.0.10(-19) erg cm, and the bending rigidity as expressed in terms of the DNA persistence length is a = 500 A. The obtained value of C agrees well with earlier estimates by Shore and Baldwin as well as by Horowitz and Wang whereas the a value is in accord with the data of Hagerman. We have found the data of Shore and Baldwin on the chain length dependence of the [delta Lk)2) value to be entirely inconsistent with our theorectical results.

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Section: Frank-kamenetskii Eta/supporting

confidence: 84%

“…Let us compare our data with the results of Shimada and Yamakawa (20,21). Since their analysis presupposes that n = L!2a is small, such a comparison is sensible only …”

Section: Resultsmentioning

confidence: 80%

Section: Theorymentioning

confidence: 99%

See 1 more Smart Citation

Torsional and Bending Rigidity of the Double Helix from Data on Small DNA Rings

Frank‐Kamenetskii

Lukashin

Anshelevich

et al. 1985

Journal of Biomolecular Structure and Dynamics

127

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“…At the other extreme, when the length of DNA separating the sites decreases, the stiffness of the DNA should hold the sites (and the proteins bound to the sites) apart and hinder loop formation. Maximal loop formation ought to occur at some intermediate loop size, much like the maximum that is seen in DNA ring closure or cyclization as a function of DNA length (5,13,14).…”

mentioning

confidence: 98%

In vivo DNA loops in araCBAD: size limits and helical repeat.

Lee

Schleif²

1989

Proc. Natl. Acad. Sci. U.S.A.

119

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Formation of a DNA loop by AraC proteins bound at the aral and araO2 sites, whose center-to-center distance is 211 base pairs, is necessary for repression of the araBAD promoter, PBAD, of Escherichia coli. To determine the upper and lower size limits of the loop, we constructed PBADreporter gene fusion plasmids with various spacings between aral and araO2 and measured their levels of expression. Spacings larger than about 500 base pairs resulted in elimination of detectable repression. No lower limit to spacing was found, suggesting that AraC protein itself possesses significant flexibility and its bending substantially aids formation of small loops. As the spacing between aral and araO2 varied, the activity of PBAD oscillated with an 11.1-base-pair periodicity, implying that the in vivo helical repeat of this DNA is 1.1 base pairs per turn.

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“…Traditional concepts hold that chromatin remodeling factors are important for this process (6), but there is a chicken-and-egg situation inherent in this scenario: how do remodeling factors access the DNA and "relax" its association with the nucleosome if the DNA is wrapped so tightly that the remodeling factors themselves cannot gain access? Because short promoter sequences are believed to be relatively stiff (12,14), it seems unlikely that transcriptional complexes, by themselves, impart sufficient energy to overcome the intrinsic rigidity of the DNA sequence, unwrapping it from the associated nucleosome. However, introduction of a dsDNA nick could serve to relax the DNA, while base oxidation products, such as 8-oxoguanine or its repair intermediate, an abasic site, introduce considerable tortional flexibility (1,11).…”

mentioning

confidence: 99%

Bending and breaking the code: dynamic changes in promoter integrity may underlie a new mechanism regulating gene expression

Gillespie¹,

Wilson²

2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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SINCE OUR FIRST BIOLOGY CLASS, we have learned that maintenance of DNA integrity is indispensable for the life of every mammalian cell. When DNA is damaged and the code cannot be properly deciphered, something significant invariably happens: mutation, evolution, disease (or at least "disease propensity"), senescence, etc. Not surprisingly, mammalian cells are endowed with complex and rather efficient surveillance mechanisms for detecting DNA damage and repairing such lesions with considerable precision. In what could be viewed as a final line of defense, changes in DNA integrity also trigger cell death pathways. Cells at risk for mutagenic events are thus eliminated before the organism suffers the consequences of having a constituent with a potentially defective genome. It seems to make good sense that the integrity of DNA is guarded at all costs.Maybe not. There is mounting evidence that reversible alterations in genetic integrity may be a part of normal, dayto-day cellular operations. In a recent provocative report, Ju and colleagues (10) found in cultured MCF-7 cells that signaldependent activation of gene transcription requires transient, topoisomerase II␤ (Topo II␤)-mediated, site-specific formation of double strand (ds) breaks in DNA. In cultured pulmonary artery endothelial and smooth muscle cells, hypoxia and other signals reported to use reactive oxygen species (ROS) as second messengers have been shown to cause reversible oxidative base modifications in nuclear DNA (8, 16). Double strand DNA breaks and oxidative DNA "damage" associated with signaling! What for?The dsDNA break discovered by Ju et al. (10) and findings of signaling-related oxidative base damage share a number of conspicuous features that may point to a common biological role. First, both kinds of "lesions" were detected in functionally significant regions of inducible genes. Using a clever adaptation of the ChIP assay, Ju et al. found dsDNA nicks in a hormone-responsive, nucleosome-associated promoter sequence of the pS2 gene. In terms of the VEGF gene hypoxic response element, we (8, 16) used ligation-mediated PCR to detect oxidative base modifications at nucleotide-resolution and found that the 3Ј-guanine of the hypoxia-inducible factor (HIF)-1 DNA binding sequence was most frequently targeted for oxidative modification in response to hypoxia and other stimuli using ROS as second messengers.Second, multiple lines of evidence suggested that the lesions in both the pS2 and VEGF promoters somehow modulated gene expression. In both instances, changes in DNA integrity were temporally related to induction of gene expression. In the case of the pS2 promoter, Ju et al. (10) demonstrated that the Topo II␤-mediated dsDNA break served as a substrate for poly[adenosine diphosphate(ADP)-ribose]polymerase-1 (PARP-1) binding, which in turn was necessary for local chromatin remodeling and transcriptional activation. In our studies, incorporation of a model abasic site at the hypoxia-modified guanine in an oligonucleotide sequence of the VEGF hypoxic re...

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DNA–topoisomer analysis on the basis of the helical wormlike chain

Cited by 19 publications

References 14 publications

Torsional and Bending Rigidity of the Double Helix from Data on Small DNA Rings

Torsional and Bending Rigidity of the Double Helix from Data on Small DNA Rings

In vivo DNA loops in araCBAD: size limits and helical repeat.

Bending and breaking the code: dynamic changes in promoter integrity may underlie a new mechanism regulating gene expression

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