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Klausnitzer, A.

Publications and source records attributed to Klausnitzer, A..

2 recordsLinked to original sources

Conformational selection drives substrate-ATP coupling in the type VI ABC transporter

The mechanism of substrate-ATP coupling is central to the function of ABC transporters. Substrates bind to the specialized transmembrane domains (TMDs), whereas ATP binding and hydrolysis occur in the conserved intracellular nucleotide-binding domains (NBDs). Efficient substrate transport requires coupling between these processes, in which the intracellular coupling helices play an essential role. Here, we probed both coupling helices of the type VI ABC transporter LptB2FG(C), the core complex responsible for intermembrane lipopolysaccharide (LPS) transport in Gram-negative bacteria, using site-specific 19F labeling and ultra-fast MAS NMR. We show that both coupling helices exist in an equilibrium among three major conformational states. Progression through the coupling cycle occurs via conformational selection, as LPS and nucleotide binding shift the conformational equilibrium, providing evidence for bidirectional communication between the TMDs and NBDs. Furthermore, the conformational distributions of the two coupling helices are asymmetric. Finally, complex formation with LptC, a unique feature of type VI ABC transporters, symmetrizes the conformational landscape of the coupling helices and facilitates transitions between conformational states, thereby enhancing the efficiency of coupling ATP hydrolysis to LPS transport. Together, our findings establish the coupling helices as dynamic allosteric elements that integrate nucleotide and substrate binding through conformational selection, providing a mechanistic framework for substrate-ATP coupling in ABC transporters.

biophysics↗

Conformational plasticity of LptC regulates lipopolysaccharide transportby the LptB2FGC complex

The outer membrane of Gram-negative bacteria is coated with lipopolysaccharide (LPS). The Lpt system maintains membrane asymmetry by transporting LPS from the inner to the outer membrane. Transport begins with the LptB2FGC complex, where the ABC transporter LptB2FG associates with LptC to extract LPS. LPS is then passed via LptA to the LptDE translocon. While LptB2FGC structures suggest an extrusion mechanism, the role of LptC remains unclear. Here, we reconstituted the complex in vitro from purified LptB2FG and LptC, and demonstrate that LptC stabilizes the complex and modulates ATPase activity. Using differential isotope labeling and solid-state NMR including dynamic nuclear polarization, we observed that the LptC transmembrane helix LptCTMH is tightly associated with the transporter in the apo state. Upon LPS or ATP binding, LptCTMH becomes dynamic, favoring cavity collapse and substrate-coupled ATPase activity. Our data support a model in which LptC acts as a mechanical transducer linking transport and energy consumption.

biophysics↗