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Delbianco, M.

Publications and source records attributed to Delbianco, M..

3 recordsLinked to original sources

Site-specific processing of phosphoethanolamine cellulose by the BcsZ cellulase reveals stochastic biofilm cellulose modification

Cellulose is a common component of bacterial biofilms where it interacts with other biopolymers to form a 3-dimensional matrix enclosing the bacteria. Synthesized and secreted by the synthase-dependent biosynthesis pathway common to many bacterial exopolysaccharides, its surface exposure depends on the presence of the periplasmic cellulase BcsZ. During export across the periplasm, E. coli and other Enterobacteriaceae modify cellulose with lipid-derived phosphoethanolamine (pEtN). How BcsZ hydrolyzes pEtN-cellulose in the periplasm is unknown and so is the native distribution pattern of pEtN on cellulose. Here, we used carbohydrate synthesis, X-ray crystallography, native mass spectrometry, and super-resolution MINFLUX nanoscopy to delineate the role of BcsZ during cellulose biosynthesis. Crystal structures of BcsZ bound to chemically synthesized pEtN cello-oligosaccharides identify how the enzyme recognizes pEtN-modified glucosyl units. Comparing mono and double substituted cellohexaoses, we identify varying binding poses that are determined by two pEtN coordination sites within the BcsZ catalytic pocket. Combined, our structural analyses reveal an ideal BcsZ cellohexaose ligand containing two pEtN modified units separated by an unmodified cellotriosyl unit. The enzyme binds and hydrolyzes this compound with substantially increased affinity and efficiency. Further, BcsZ digestion of native pEtN cellulose combined with native mass spectrometry analyses reveals the stochastic distribution of pEtN on biofilm cellulose. Additionally, MINFLUX co-localization of BcsZ with other components of the biosynthetic complex demonstrates the random distribution of BcsZ across the periplasm. Our data suggest BcsZ functions independently of the biosynthetic complex to clear mislocalized pEtN cellulose from the periplasm.

biophysics↗

Chitinase-3-like protein 1 decodes chitosan acetylation patterns into toll-like receptor 2 signaling through heparan sulfate

Chitinase-3-like protein 1 (CHI3L1), which is associated with a wide range of inflammatory diseases, lacks chitinase activity but retains the ability to bind chitin and chitosan. Chitin is a major component of fungal cell walls, whereas chitosan is used in biomedicine. In addition to chitosan, CHI3L1 has been proposed to interact with heparan sulfate (HS), a highly sulfated glycosaminoglycan on mammalian cell surfaces. Here, we investigated how interactions with chitosan and HS regulate the pro-inflammatory activity of CHI3L1. Mapping of the chitin-binding cleft revealed preferential binding of CHI3L1 to chitosans with a regular acetylation pattern that, together with CHI3L1, promoted toll-like receptor 2 signaling. We further identified a dominant HS-binding site that recognizes a distinct HS sulfation code containing a coherent motif of N- and 6-O-sulfations. Mutation of this HS-binding site or impaired HS biosynthesis prevented CHI3L1 accumulation at the cell surface and abolished CHI3L1-mediated cell activation. Together, our findings establish HS as a critical co-receptor for CHI3L1 and reveal a pro-inflammatory cross-talk between HS, CHI3L1, and chitosan that may contribute to host defense against fungal pathogens and responses to chitosan-based biomaterials. These findings identify HS- and chitosan-dependent CHI3L1 signaling as a potential target for modulating inflammatory responses.

Molecular Biology↗

Role of van der Waals, electrostatic, and hydrogen-bond interactions for the relative stability of cellulose Iβ and II crystals

Naturally occuring cellulose I{beta} with its characteristic parallel orientation of cellulose chains is less stable than cellulose II, in which neighbouring pairs of chains are oriented antiparallel to each other. While the distinct hydrogen-bond patterns of these two cellulose crystal forms are well established, the energetic role of the hydrogen bonds for crystal stability, in comparison to the van der Waals and overall electrostatic interactions in the crystals, is a matter of current debate. In this article, we investigate the relative stability of cellulose I{beta} and II in energy minimizations with classical force fields. We find that the larger stability of cellulose II results from clearly stronger electrostatic interchain energies that are only partially compensated by stronger van der Waals interchain energies in cellulose I{beta}. In addition, we show that a multipole description of hydrogen bonds that includes the whole COH groups of donor and acceptor oxygen atoms leads to consistent interchain hydrogen-bond energies that account for roughly 70% and 75% of the interchain electrostatics in cellulose I{beta} and II, respectively.

biophysics↗