In this new study published in PNAS, Haoran and Lydia, together with collaborators in the Weitao Yang and Pei Zhou labs at Duke and the Alexey Silakov lab at Penn State, uncovered a substrate-triggered radical initiation. Using radical SAM enzyme MoA as a model, they discovered that MoaA uses its conformationally flexible C-terminal tail with two conserved Gly residues (GG motif) at the C-terminus as a sensor to detect substrate guanosine 5′-triphosphate (GTP) binding and trigger reductive SAM cleavage. Importantly, they also found that mutations disrupting this regulatory mechanism lead to Moco deficiency disease in humans. Congratulations to Haoran and Lydia!
Department of Biochemistry, Duke University School of Medicine
