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Temperate phages promote colicin‐dependent fitness of S almonella enterica serovar T yphimurium
Author(s) -
Nedialkova Lubov P.,
Sidstedt Maja,
Koeppel Martin B.,
Spriewald Stefanie,
Ring Diana,
Gerlach Roman G.,
Bossi Lionello,
Stecher Bärbel
Publication year - 2016
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.13077
Subject(s) - colicin , biology , bacteriocin , microbiology and biotechnology , escherichia coli , salmonella enterica , bacteriophage , lysis , siphoviridae , competition (biology) , genetics , biochemistry , gene , antimicrobial , ecology
Summary Bacteria employ bacteriocins for interference competition in microbial ecosystems. Colicin Ib ( ColIb ), a pore‐forming bacteriocin, confers a significant fitness benefit to S almonella enterica serovar T yphimurium ( S . Tm ) in competition against commensal E scherichia coli in the gut. ColIb is released from S . Tm into the environment, where it kills susceptible competitors. However, colicin‐specific release proteins, as they are known for other colicins, have not been identified in case of ColIb . Thus, its release mechanism has remained unclear. In the current study, we have established a new link between ColIb release and lysis activity of temperate, lambdoid phages. By the use of phage‐cured S . Tm mutant strains, we show that the presence of temperate phages and their lysis genes is necessary and sufficient for release of active ColIb into the culture supernatant. Furthermore, phage‐mediated lysis significantly enhanced S . Tm fitness in competition against a ColIb ‐susceptible competitor. Finally, transduction with the lambdoid phage 933W rescued the defect of E . coli strain MG1655 with respect to ColIb release. In conclusion, ColIb is released from bacteria in the course of phage lysis. Our data reveal a new mechanism for colicin release and point out a novel function of temperate phages in enhancing colicin‐dependent bacterial fitness.