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Biology subjects

Kossmann, B. R.

Publications and source records attributed to Kossmann, B. R..

2 recordsLinked to original sources

Orchestrated metal ion repositioning defines the dynamic catalytic strategy of the essential DNA repair nuclease APE1

Human AP-endonuclease 1 (APE1) is a vital enzyme in the base excision repair pathway that protects genome stability by eliminating ubiquitous abasic DNA lesions. Despite its importance and therapeutic potential, how APE1 achieves high specificity and single-metalion catalytic efficiency remains unclear. Here, we present a high-resolution structure of the APE1-DNA Michaelis complex coordinated with physiological cofactor Mg2+. Integrating this snapshot with ab initio molecular dynamics and metadynamics simulations reveals a novel "moving metal ion" mechanism in which Mg2+ undergoes orchestrated repositioning to trigger a concerted catalytic reaction, bypassing the formation of an associative pentavalent intermediate. This distinct catalytic strategy, driven by concerted active-site reorganization, enables APE1 to efficiently process damaged DNA using only one metal ion cofactor. A previously unrecognized hydrogen-bonding network couples catalytic water activation to the metal ion movement - two events that strikingly occur on opposite sides of the active site. These findings provide a blueprint for how enzymes synchronize distal active site rearrangements with transition state formation. Our results further suggest that effective AI-targeted inhibitor design should develop capacities to predict mechanistically critical non-canonical rotamers and transient hydrogen-bonding networks. Our combined findings offer a foundation for the design of inhibitors targeting APE1 overexpression in cancer.

biochemistry↗

Engineering a Cell-Based Orthogonal Ubiquitin Transfer Cascade for Profiling the Substrates of RBR E3 Parkin

The E3 ubiquitin (UB) ligase Parkin utilizes a Ring-Between-Ring (RBR) domain to mediate the transfer of UB to its substrates to regulate diverse cellular functions, including mitochondrial quality control, cell cycle progression, metabolism programming, and the establishment of synaptic functions. Mutations affecting the E3 ligase activity of Parkin are associated with cancer and Parkinsons disease (PD). An essential role of Parkin is to synthesize UB chains on the surface of damaged mitochondria to initiate mitophagy. Still, it is not clear how Parkin carries out other biological functions through the ubiquitination of its downstream targets in the cell. We hypothesized that a comprehensive substrate profile of Parkin would facilitate the discovery of ubiquitination pathways underpinning its multifaceted roles in cell regulation and reveal mechanistic linkages between Parkin malfunction and disease development. Here, we used phage display to assemble an orthogonal ubiquitin transfer (OUT) cascade of Parkin that can exclusively deliver an engineered UB mutant (xUB) to Parkin and its substrates in living cells. We then generated a substrate profile of Parkin by purifying xUB-conjugated proteins from cells and identifying them by proteomics. The OUT screen identified Parkin substrates involved in DNA replication, protein translation, intracellular protein transport, and rhythmic regulation. Based on previous literature implicating alterations in membrane vesicle trafficking in PD, we verified Parkin-catalyzed ubiquitination of Rab GTPases (Rab1a, Rab5a, Rab5c, Rab7a, Rab8a, Rab10, an Rab13) as well as CDK5, with reconstituted ubiquitination reactions in vitro and in cells. We also found chemical-induced stimulation of mitophagy enhanced Parkin-mediated ubiquitination of Rab proteins. These findings demonstrate that the OUT cascade of Parkin can serve as an empowering tool for identifying Parkin substrates to elucidate its cellular functions.

biochemistry↗