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Hernandez, C. R.

Publications and source records attributed to Hernandez, C. R..

2 recordsLinked to original sources

Substrate-induced assembly and functional mechanism of the bacterial membrane protein insertase SecYEG-YidC

The Sec translocon and the YidC/Oxa1-type insertases universally mediate biogenesis of -helical membrane proteins, but the molecular basis of their cooperation has remained disputed. Recent discoveries of multi-subunit insertases assembled at the back of the translocon in fungi and higher eukaryotes have raised the question about the architecture and mechanism of the putative bacterial ortholog SecYEG-YidC. Here, we combine cryogenic electron microscopy with cell-free protein synthesis to visualize biogenesis of SecYEG/YidC-dependent multipass membrane protein NuoK. We demonstrate that the nascent chain of NuoK does not enter the lateral gate of SecYEG, but crosses over the translocon towards its back side, whereto YidC is recruited in the nascent chain-dependent manner. The SecY-YidC interface promotes folding of the transmembrane helices prior their insertion, in agreement with thermodynamic principles of membrane protein folding. YidC forms extensive contacts with the nascent chain, suggesting its key role in the insertion event. Our data provide detailed insights on the insertase machinery, suggest the evolutionary conservation of the gate-independent insertion route, and offer an expanded view on membrane protein biogenesis.

biochemistry↗

Assembly and dynamics of the outer membrane exopolysaccharide transporter PelBC of Pseudomonas aeruginosa

The infamous opportunistic pathogen Pseudomonas aeruginosa enhances its virulence and antibiotic resistance upon formation of durable biofilms. The biofilm stability is mediated by its matrix built of secreted exopolysaccharides, eDNA, and structural proteins. Exopolysaccharides of P. aeruginosa - Pel, Psl and alginate - have the highest biomedical relevance, but the mechanisms behind their synthesis and secretion are poorly understood. Here, we employ cryogenic electron microscopy to resolve the 2.5 [A] structure of the outer membrane complex PelBC for Pel exopolysaccharide, which is uniquely composed of the membrane-embedded {beta}-barrel PelB and the asymmetrical ring of 12 lipoproteins PelC at the periplasmic interface. The assembly captured in the lipid-based nanodisc is stabilized by electrostatic contacts of PelC with the periplasmic loops of PelB and multiple interactions with PelB N-terminal helical domains. Within the membrane, the resolved acyl chains of the PelC lipoproteins are alternated by the tryptophan residues immersed into the lipid leaflet, thus offering a stable anchoring architecture. The highly anionic interior of the PelB {beta}-barrel is sealed by three loops at the extracellular side, where the short Plug-S loop is aligned with the periplasmic helical scaffold, being the potential gating element for the Pel exopolysaccharide tunneling. Molecular dynamic simulations of PelB in native-like membrane environments suggest that Plug-S is sufficiently flexible to open a tunnel, and so serve as a gate. The gating model is further supported by single-channel conductivity measurements, which identify two conductance states of PelB. Via mutational analysis we confirm that Plug-S mediates opening of a narrow tunnel, as required for the controlled exopolysaccharide transport. Our structural and functional analysis of the pathogenicity-relevant complex offer a detailed and comprehensive view on this unique machinery and suggest the route taken by the exopolysaccharide at the final secretion step.

biophysics↗