Deciphering the chemical basis of fluorescence of a selenium-labeled uracil probe when bound at the bacterial ribosomal A-site.

We unveil in this work the main factors that govern the turn-on/off fluorescence of a Se-modified uracil probe at the ribosomal RNA A-site. Whereas the constraint into an 'in-plane' conformation of the two rings of the fluorophore is the main driver for the observed turn-on fluorescence emission in the presence of the antibiotics paromomycin, the electrostatics of the environment plays a minor role during the emission process. Our computational strategy clearly indicates that in the absence of paramomycin, the probe prefers conformations that show a dark S1 electronic state with participation of npi* electronic transition contributions between the selenium atom and the pi-system of the uracil moiety.