The study reveals how the radical SAM enzyme MoaA controls essential yet potentially dangerous radical chemistry by using its flexible C-terminal tail to sense the correct substrate and safely trigger radical formation. Disruption of this mechanism in humans leads to a fatal disease. This discovery also provides a testable model for radical initiation across the radical SAM enzyme superfamily. Read “How an Enzyme Controls Essential Radical Chemistry — and Its Links to Human Disease” on the PNAS Showcase.
Department of Biochemistry, Duke University School of Medicine
