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Charro, D.

Publications and source records attributed to Charro, D..

2 recordsLinked to original sources

Tertiary and quaternary structure remodeling by occupancy of the substrate binding pocket in a large glutamate dehydrogenase

Glutamate dehydrogenases (GDHs) catalyze the oxidative deamination of L-glutamate to 2-oxoglutarate using NAD(P)+ as a cofactor. The large type of GDHs (L-GDHs) displays a dynamic homotetrameric architecture that alternates between open and closed states. However, the catalytic mechanism and the functional relevance of the large conformational changes in L-GDHs remain poorly understood. Here, we use cryo-EM to investigate the structure and the conformational landscape of the mycobacterial L-GDH composed of 180 kDa subunits (mL-GDH180) when incubated with L-glutamate and NAD+. Classification of the heterogeneous population of tetramers reveals opening-closing motions and sorting of individual subunits resolves the occupancy of the cofactor and substrate binding pockets. Cryo-EM maps show that ligand binding to the glutamate binding pocket is accompanied by structural changes in a region approximately two nanometers away from the active site, leading to the formation of a previously undetected interaction between the catalytic domains of neighboring subunits in mL-GDH180 closed tetrameric states. Our findings indicate that the occupancy of the substrate binding site of mL-GDH180 is linked to a remodeling of both the tertiary and quaternary structure of the enzyme. STATEMENT FOR A BROADER AUDIENCEThis work reveals how the binding of L-glutamate and NAD+ reshapes the architecture of a large glutamate dehydrogenase, linking active site occupancy to long-range structural remodeling. By capturing previously unseen conformational transitions with cryo-electron microscopy, we provide insights into the molecular logic of enzyme function in mycobacteria. These findings establish a framework to understand how structural plasticity supports metabolic control.

molecular biology↗

Solvent-induced allosteric transition of the Hepatitis C virus human cellular receptor CD81 large extracellular loop

CD81 is a tetraspanin receptor that clusters into microdomains to mediate cell signalling processes. CD81 is also one of the four primary cellular receptors of the Hepatitis C virus (HCV). Previous structural studies on the -helical CD81 large-extracellular-loop domain (CD81LEL) have shown that it can adopt different conformations (from closed to open), likely depending on the environmental conditions. This conformational plasticity has been implicated in the endosomal fusion of HCV upon entry. However, the precise mechanism governing the CD81LEL plasticity has remained elusive so far. Here, by combining molecular dynamics simulations and circular dichroism experiments on wt-CD81LEL and two mutants at different endosomal pH conditions, pH 5.5 and pH 4.6, we show that the modulation of the solvation shell governs the plasticity of CD81LEL. The primarily implicated residues are D139 and E188, respectively, located near a loop preceded by a helix. At acidic conditions, their interaction with water is reduced, causing a re-ordering of the water molecules, and thus triggering the dynamics of CD81LEL. However, mutations E188Q and D139N retain the solvation shell and restrict the conformational space that the head subdomain can explore. We propose that residues E188 and D139 control the solvent-induced allosteric transition of the CD81LEL domain. This mechanism might play a role in other cellular receptors that function along the endosomal pathway. Popular SummaryUnderstanding the cellular mechanisms that are exploited by viruses to infect their host is key for the development of therapeutics. Here, in the context of Hepatitis C Virus infection we report the mechanism that governs the plasticity of the extra-cellular domain of tetraspanin CD81, one of the major cellular receptors of this virus. The mechanism proposed here is a novel form of solvent-induced allosteric transition in proteins mediated by two antenna residues located in the head subdomain of CD81. We propose that it could serve as a pH sensing strategy to time the endosomal pathway and trigger a signal at the right time for HCV fusion.

biophysics↗