RT Journal Article
T1 The role of PemIK (PemK/PemI) type II TA system from Klebsiella pneumoniae clinical strains in lytic phage infection.
A1 Bleriot, Ines
A1 Blasco, Lucia
A1 Pacios, Olga
A1 Fernandez-Garcia, Laura
A1 Ambroa, Anton
A1 Lopez, Maria
A1 Ortiz-Cartagena, Concha
A1 Cuenca, Felipe Fernandez
A1 Oteo-Iglesias, Jesus
A1 Pascual, Alvaro
A1 Martinez-Martinez, Luis
A1 Domingo-Calap, Pilar
A1 Wood, Thomas K
A1 Tomas, Maria
AB Since their discovery, toxin-antitoxin (TA) systems have captivated the attention of many scientists. Recent studies have demonstrated that TA systems play a key role in phage inhibition. The aim of the present study was to investigate the role of the PemIK (PemK/PemI) type II TA system in phage inhibition by its intrinsic expression in clinical strains of Klebsiella pneumoniae carrying the lncL plasmid, which harbours the carbapenemase OXA-48 and the PemK/PemI TA system. Furthermore, induced expression of the system in an IPTG-inducible plasmid in a reference strain of K. pneumoniae ATCC10031 was also studied. The results showed that induced expression of the whole TA system did not inhibit phage infection, whereas overexpression of the pemK toxin prevented early infection. To investigate the molecular mechanism involved in the PemK toxin-mediated inhibition of phage infection, assays measuring metabolic activity and viability were performed, revealing that overexpression of the PemK toxin led to dormancy of the bacteria. Thus, we demonstrate that the PemK/PemI TA system plays a role in phage infection and that the action of the free toxin induces a dormant state in the cells, resulting in inhibition of phage infections.
PB Nature Publishing Group
YR 2022
FD 2022-02-21
LK http://hdl.handle.net/10668/19594
UL http://hdl.handle.net/10668/19594
LA en
NO Bleriot I, Blasco L, Pacios O, Fernández-García L, Ambroa A, López M, Ortiz-Cartagena C, et al. The role of PemIK (PemK/PemI) type II TA system from Klebsiella pneumoniae clinical strains in lytic phage infection. Sci Rep. 2022 Mar 16;12(1):4488
NO Tis study was funded by grant PI19/00878 awarded to M. Tomás within the State Plan for R+D+I 2013-2016 (National Plan for Scientifc Research, Technological Development and Innovation 2008-2011) and co-fnancedby the ISCIII-Deputy General Directorate for Evaluation and Promotion of Research—European Regional Development Fund "A way of Making Europe" and Instituto de Salud Carlos III FEDER, Spanish Network for the Research in Infectious Diseases (REIPI, RD16/0016/0001, RD16/0016/0006 and RD16/CIII/0004/0002) and by the Study Group on Mechanisms of Action and Resistance to Antimicrobials, GEMARA (SEIMC, http://www.seimc.org/). M. Tomás was fnancially supported by the Miguel Servet Research Programme (SERGAS and ISCIII). I. Bleriot was fnancially supported by pFIS program (ISCIII, FI20/00302). O. Pacios and M. López was fnancially supported by a grant IN606A-2020/035 and IN606B-2018/008, respectively (GAIN, Xunta de Galicia) and M. Gonzalez-Bardanca was fnancially supported by the Rio Hortega program (ISCIII, CM20/00198).
DS RISalud
RD Apr 7, 2025