bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.05.01.722179

Phylogenetic Analysis and Structural Evaluation of Staphylococcus aureus Serine-Aspartate Repeat-Containing Protein D with a Focus on Periprosthetic Joint Infection

Abstract

Serine-aspartate repeat-containing protein D (SdrD) is a Staphylococcus aureus cell wall-anchored, calcium-binding adhesin member of the MSCRAMM Sdr subfamily that may contribute to bacterial adhesion and virulence. S. aureus is the most common cause of periprosthetic joint infection (PJI). Population-level distribution and sequence diversity of SdrD among clinical PJI isolates have not been systematically characterized, and the SdrD binding mechanism is still not well understood. To address these gaps, sdrD alleles were queried across 156 newly sequenced PJI isolates and compared to publicly available S. aureus genomes, and nucleotide- and protein-level phylogenies of the sdrCDE locus constructed. The SdrD crystal structure from S. aureus JH1 was determined, with solution small-angle X-ray scattering (SAXS) and molecular dynamics (MD) simulations, and assessment of conformational changes with calcium depletion. Three dominant sdrD subtypes were defined, associating with USA300, JH1, and TCH60; the JH1 sdrD subtype was predominant among PJI isolates. Structural studies showed that the conformation of individual domains and interdomain organization of the multidomain SdrD have limited flexibility in solution, and that the calcium-binding B domain retains its core fold under conditions of calcium depletion. Together, the findings presented support functional diversification among Sdr family members in mediating host attachment and inform a re-evaluation of the ligand-binding mechanism previously proposed for SdrD. AUTHOR SUMMARYStaphylococcus aureus is the leading cause of infections that develop around joint implants (periprosthetic joint infection, PJI). This bacterium has a large arsenal of surface proteins that allow it to stick to human tissues and implanted devices. This work focused on one such protein, SdrD, which has been linked to implant-associated infections but the structure and diversity of which among patients with PJI had not been well characterized. The genetic sequences of SdrD were analyzed across thousands of bacterial genomes, including those from patients with PJI. Distinct genetic variants of the protein were found, one of which was particularly common with PJI. The three-dimensional structure of SdrD was determined at atomic resolution and solution small-angle X-ray scattering (SAXS) and molecular dynamics used to study how it moves and responds to changes in its environment. Contrary to what was previously described, SdrD was shown to be relatively rigid. These findings change how SdrDs mechanism of action should be considered, potentially informing design strategies to block bacterial attachment before infection takes hold.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Joachimiak, A., Tan, K., O'Connor, K. A., Zhou, X., Gade, P., Garcia, E., Tan, A., Nijhawan, A., Endres, M., Kim, Y., Greenwood-Quaintance, K., Patel, R.. 2026-05-05. Phylogenetic Analysis and Structural Evaluation of Staphylococcus aureus Serine-Aspartate Repeat-Containing Protein D with a Focus on Periprosthetic Joint Infection. https://doi.org/10.64898/2026.05.01.722179

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Design of colipids with controlled lateral distance of head group moieties for targeting strategies in the field of lipid-based nanoparticles

Lipid nanoparticles and liposomes are nanoparticle drug formulations which are firmly established in clinics. In order to expand their application and improve efficacy, surface modifications can be a key strategy, especially for cell specific targeting. Targeting can be achieved by integrating ligand functionalized lipids or lipidoids on the nanoparticle surface. In this case, not solely the targeting ligand itself, but also the structure of the whole targeting lipid/lipidoid can affect the interaction of the targeting ligand with the binding motive on cells. Especially, distal spacer structures between lipid anchor and ligand unit, often composed of polyethylene glycol chains, provide a certain distance of the ligand from the nanoparticle surface. A concept which is currently neglected is the control of the lateral distance between ligand structures on the nanoparticle. Herein we investigated the possibility to design lipidoids with a lateral spacer composed of polyethylene glycol units. We synthesized and characterized different lipidoids which provide a primary amine in the head group for possible ligand coupling. In our model lipidoids the head groups were functionalized with a paramagnetic probe to apply electron paramagnetic resonance (EPR) methods for the characterization of the lipidoid interaction with model nanoparticles, in our case liposomes. Continuous wave EPR was used to study the efficiency of the novel lipidoids to integrate into lipid bilayers of model liposomes, which was shown to depend on lipidoid structure and liposome composition. Furthermore, using double electron-electron resonance (DEER), we observed lipidoid conformational changes occurring upon integration into liposomes.

biophysics↗

Binding mechanisms of therapeutic antibodies to human claudin-18.2

Claudin-18.2 (CLDN18.2) is a tight junction component with highly restricted expression in the paracellular space of nonmalignant gastric epithelial cells. It becomes accessible on tumor cell surface during malignant transformation, making CLDN18.2 an attractive target for targeted therapies against gastric cancer. Recently, zolbetuximab has become the first FDA-approved monoclonal antibody that targets CLDN18.2 in advanced gastric cancer, and others like osemitamab have entered phase 3 clinical trials. However, the high-resolution structure of CLDN18.2 is lacking, and how CLDN18.2 is recognized by therapeutic antibodies remains undefined. Here, we report cryo-EM structures of human claudin-18.2 (hCLDN18.2) in complex with the Fab fragments of zolbetuximab and osemitamab, revealing the structure of hCLDN18.2 and its binding mechanism to the therapeutic antibodies. Further analyses reveal that three residues in the first extracellular loop of hCLDN18.2 that are different from human claudin-18.1 (hCLDN18.1) play a critical role in antibody binding. Our data elucidate the structural basis for selective binding of therapeutic antibodies to hCLDN18.2, which should aid rational design of next-generation immunotherapies targeting hCLDN18.2.

biophysics↗

Structural relationships between the SLC12 cotransporter C-terminal domain, universal stress proteins and adenylating enzymes

Several SLC12 cotransporters bind ATP in a cytoplasmic C-terminal domain (CTD). We analysed 16,192 CTD-containing SLC12 sequences and compared 42,845 representative structures to examine the relationship between this nucleotide site, universal stress proteins (USPs) and adenylating enzymes. In phosphorylated NKCC1, D891 and D927 lie near the ATP phosphate chain, while R801 and K889 form a basic phosphate-binding clamp. NKCC1 retains this arrangement, whereas KCC paralogs replace or lose several corresponding groups. In structural comparisons with USP and adenylating-enzyme references, both CTD lobes score between universal stress proteins and EC-annotated domains, and the two lobes form separate lineages that include bacterial transporters. Lobe-specific and nucleotide-frame comparisons place ATP in the corresponding structural region used for -phosphate chemistry by catalytic members of this fold. Published work on UspG provides a precedent for protein-bound AMP in a natural USP. In the examined SLC12 structures and USP models, candidate protein hydroxyls lack an in-line geometry for attack at ATP P. Protein adenylation would require a change in protein or nucleotide geometry, or a different acceptor. These results define a structural basis for testing conditional protein adenylation at SLC12 nucleotide sites. The required evidence is a covalent protein-AMP adduct, identification of its acceptor and measurement of the expected pyrophosphate coproduct, with soluble nucleotide analysis to distinguish accompanying ATP reactions.

biophysics↗