Origin of the intrinsic rigidity of DNA.
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 ((me)A). Upon addition of (me)A, 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 dT(n)-dA(n) homopolymer derives from base pair stacking effects, with phosphate-phosphate interactions contributing relatively little to net helix rigidity at moderate salt concentrations.
Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, 4200 East Ninth Avenue, Denver, CO 80262, USA.
Janine B
JB
Mills
Paul J
PJ
Hagerman
D000225:Adenine / Q000031:analogs & derivatives* / Q000737:chemistry; D020029:Base Pairing; D001483:Base Sequence; D004247:DNA / Q000737:chemistry*; D004277:DNA, Single-Stranded / Q000737:chemistry; D012399:Rotation; D013941:Thymine / Q000737:chemistry
D000225:Adenine; D004247:DNA; D004277:DNA, Single-Stranded; D013941:Thymine; C000730567:6-methyladenine