Electronic Relaxation Mechanism of 9-Methyl-2,6-Diaminopurine and 2,6-Diaminopurine-2’-Deoxyribose in Solution

Prolonged ultraviolet exposure results in the formation of adducts such as the cyclobutene pyrimidine dimers (CPDs) in RNA despite the established photostability of the nucleic acids. Therefore, prebiotic photolesion repair mechanisms should have played an important role in the maintenance of the structural integrity of primitive nucleic acids. 2,6-Diaminopurine (2,6DAP) is a prebiotic nucleobase that has been demonstrated to repair CPDs with high efficiency when incorporated into nucleic acid polymers. We investigate the electronic deactivation pathways of 2,6-diaminopurine-2’-deoxyriside (2,6DAP-d) and 9-methyl-2,6-diaminopurine (9Me2,6DAP) in acetonitrile and aqueous solution to shed light on the photophysical and excited state properties of the 2,6DAP chromophore. Spectroscopic measurements, enhanced with electronic-structure calculations, evidence that both are photostable prebiotic compounds that exhibit nearly identical deactivation mechanisms upon population of the S1(ππ* La) state at 290 nm. The electronic relaxation mechanism involves deactivation through two reaction coordinates (C2- and C6-coordinates) and >99% of the excited state population decays through non-radiative pathways involving two conical intersections with the ground state. The results support the idea that 2,6DAP should have accumulated in significant quantities during prebiotic times to participate in the formation of non-canonical RNA oligonucleotides and play a significant role in the protection of the prebiotic genetic code.