Abstract

Exposure of genomic, single-stranded DNA (ssDNA) during transcription and replication creates opportunities for the formation of inappropriate secondary structures. CTG repeat has been shown to form stable secondary structures that are the cause of inherited human genetic disease related to the myotonic dystrophy. Here, we investigated the role of SWCNT and BNNT in preventing CTG repeat using molecular dynamics (MD) simulations. The assessment of the simulations reveals that the ssDNA undergoes rapid conformational changes and wrap around the SWNTs via π-stacking interactions between SWNT’s wall and the nucleobases of the ssDNA. The ssDNA is observed to spontaneously wrap around SWNTs into compact right-handed helice within a few nanoseconds. Helical wrapping is driven by the electrostatic and torsional interactions within the sugar–phosphate backbone that result in ssDNA wrapping from the 3′end to the 5′end. Our computations demonstrate that the binding strength of the ssDNA to the SWCNT is substantially greater than to the BNNT. These findings would enable providing new avenues for therapeutic interventions in of myotonic dystrophy and potentially other triplet repeat disorders.

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