EMD-42086

Tomography
EMD-42086 Deposition: 22/09/2023
Map released: 12/06/2024
Last modified: 26/06/2024
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EMD-42086

Representative tomogram of Enterococcus faecium SagA complementation strain

EMD-42086

Tomography
EMD-42086 Deposition: 22/09/2023
Map released: 12/06/2024
Last modified: 26/06/2024
Overview Sample Experiment Validation Volume Browser Additional data Links
Sample Organism: Enterococcus faecium
Sample: Enterococcus faecium WT Com15
Raw data: EMPIAR-11692

Deposition Authors: Hang HC , Park D
Secreted antigen A peptidoglycan hydrolase is essential for Enterococcus faecium cell separation and priming of immune checkpoint inhibitor therapy.
PUBMED: 38857064
DOI: doi:10.7554/eLife.95297
ISSN: 2050-084X
Abstract:
Enterococcus faecium is a microbiota species in humans that can modulate host immunity (Griffin and Hang, 2022), but has also acquired antibiotic resistance and is a major cause of hospital-associated infections (Van Tyne and Gilmore, 2014). Notably, diverse strains of E. faecium produce SagA, a highly conserved peptidoglycan hydrolase that is sufficient to promote intestinal immunity (Rangan et al., 2016; Pedicord et al., 2016; Kim et al., 2019) and immune checkpoint inhibitor antitumor activity (Griffin et al., 2021). However, the functions of SagA in E. faecium were unknown. Here, we report that deletion of sagA impaired E. faecium growth and resulted in bulged and clustered enterococci due to defective peptidoglycan cleavage and cell separation. Moreover, ΔsagA showed increased antibiotic sensitivity, yielded lower levels of active muropeptides, displayed reduced activation of the peptidoglycan pattern-recognition receptor NOD2, and failed to promote cancer immunotherapy. Importantly, the plasmid-based expression of SagA, but not its catalytically inactive mutant, restored ΔsagA growth, production of active muropeptides, and NOD2 activation. SagA is, therefore, essential for E. faecium growth, stress resistance, and activation of host immunity.