biostudies-literatureKlupt SNCI NIH HHSScripps Research InstituteNational Institutes of HealthNIH HHSRP95297https://www.ebi.ac.uk/biostudies/studies/S-EPMC11164530biostudies-literatureUnknown13<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. MoreoeLifeSecreted antigen A peptidoglycan hydrolase is essential for <i>Enterococcus faecium</i> cell separation and priming of immune checkpoint inhibitor therapy.PMC11164530David C. Fairchild Endowed FellowshipR01 CA245292Start-up fundsS10 OD032467CA245292Chodisetti PKZhang XGrotjahn DBoyd TFam KTMehmood AHang HCPark DKlupt SfalseSecreted antigen A peptidoglycan hydrolase is essential for <i>Enterococcus faecium</i> cell separation and priming of immune checkpoint inhibitor therapy.<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. Moreo2024-01-01T00:00:00Z2024 Jun2026-07-15T13:50:29.128Z2026-07-05T03:11:20.426ZS-EPMC111645303885706410.7554/eLife.95297