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Nucleic Acids Research 2004 32(13):4055-4059; doi:10.1093/nar/gkh740
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Published online 2 August 2004

Nucleic Acids Research, Vol. 32 No. 13 © Oxford University Press 2004; all rights reserved

Origin of the intrinsic rigidity of DNA

Janine B. Mills and Paul J. Hagerman1,*

Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, 4200 East Ninth Avenue, Denver, CO 80262, USA and 1 Department of Biochemistry and Molecular Medicine, School of Medicine, University of California, One Shields Avenue, Davis, CA 95616, USA

* To whom correspondence should be addressed. Tel: +1 530 754 7266; Fax: +1 530 754 7269; Email: pjhagerman{at}ucdavis.edu

Received May 21, 2004; Revised and Accepted July 15, 2004

The intrinsic rigidities of DNA and RNA helices are generally thought to arise from some combination of vertical base-stacking interactions and intra-helix phosphate–phosphate charge repulsion; however, the relative contributions of these two types of interaction to helix rigidity have not been quantified. To address this issue, we have measured the rotational decay times of a ‘gapped-duplex’ DNA molecule possessing a central, single-stranded region, dT24, before and after addition of the free purine base, N6-methyladenine (meA). Upon addition of meA, the bases pair with the T residues, forming a continuous stack within the gap region. Formation of the gapped duplex is accompanied by a nearly 2-fold increase in decay time, to values that are indistinguishable from the full duplex control for monovalent salt concentrations up to 90 mM. These results indicate that at least 90% of the rigidity of the dTn–dAn homopolymer derives from base pair stacking effects, with phosphate–phosphate interactions contributing relatively little to net helix rigidity at moderate salt concentrations.


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