{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Klupt S"],"funding":["NCI NIH HHS","Scripps Research Institute","National Institutes of Health","NIH HHS"],"pagination":["RP95297"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11164530"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["<i>Enterococcus faecium</i> 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 <i>E. faecium</i> 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 <i>E. faecium</i> were unknown. Here, we report that deletion of <i>sagA</i> impaired <i>E. faecium</i> growth and resulted in bulged and clustered enterococci due to defective peptidoglycan cleavage and cell separation. Moreo"],"journal":["eLife"],"pubmed_title":["Secreted antigen A peptidoglycan hydrolase is essential for <i>Enterococcus faecium</i> cell separation and priming of immune checkpoint inhibitor therapy."],"pmcid":["PMC11164530"],"funding_grant_id":["David C. Fairchild Endowed Fellowship","R01 CA245292","Start-up funds","S10 OD032467","CA245292"],"pubmed_authors":["Chodisetti PK","Zhang X","Grotjahn D","Boyd T","Fam KT","Mehmood A","Hang HC","Park D","Klupt S"],"additional_accession":[]},"is_claimable":false,"name":"Secreted antigen A peptidoglycan hydrolase is essential for <i>Enterococcus faecium</i> cell separation and priming of immune checkpoint inhibitor therapy.","description":"<i>Enterococcus faecium</i> 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 <i>E. faecium</i> 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 <i>E. faecium</i> were unknown. Here, we report that deletion of <i>sagA</i> impaired <i>E. faecium</i> growth and resulted in bulged and clustered enterococci due to defective peptidoglycan cleavage and cell separation. Moreo","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-07-15T13:50:29.128Z","creation":"2026-07-05T03:11:20.426Z"},"accession":"S-EPMC11164530","cross_references":{"pubmed":["38857064"],"doi":["10.7554/eLife.95297"]}}