Escherichia coli EC93 deploys two plasmid-encoded class I contact-dependent growth inhibition systems for antagonistic bacterial interactions

The phenomenon of contact-dependent growth inhibition (CDI) and the genes required for CDI ( ) were identified and isolated in 2005 from an isolate (EC93) from rats. Although the locus has been the focus of extensive research during the past 15 years, little is known about the EC93 isolate from whic...

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Bibliographic Details
Published in:Microbial genomics 2021-03, Vol.7 (3)
Main Authors: Wäneskog, Marcus, Halvorsen, Tiffany, Filek, Klara, Xu, Feifei, Hammarlöf, Disa L, Hayes, Christopher S, Braaten, Bruce A, Low, David A, Poole, Stephen J, Koskiniemi, Sanna
Format: Article
Language:English
Subjects:
competition
contact-dependent growth inhibition
Escherichia coli
Escherichia coli - genetics
Escherichia coli - growth & development
Escherichia coli - metabolism
Escherichia coli Proteins - genetics
Escherichia coli Proteins - metabolism
genome
Genome, Bacterial
Membrane Proteins - genetics
Membrane Proteins - metabolism
Microbial Interactions
Plasmids - genetics
Plasmids - metabolism
regulation
toxic potency
toxin
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Summary:The phenomenon of contact-dependent growth inhibition (CDI) and the genes required for CDI ( ) were identified and isolated in 2005 from an isolate (EC93) from rats. Although the locus has been the focus of extensive research during the past 15 years, little is known about the EC93 isolate from which it originates. Here we sequenced the EC93 genome and find two complete and functional loci (including the previously identified locus), both carried on a large 127 kb plasmid. These systems are differentially expressed in laboratory media, enabling EC93 to outcompete cells lacking cognate immunity genes. The two CDI systems deliver distinct effector peptides that each dissipate the membrane potential of target cells, although the two toxins display different toxic potencies. Despite the differential expression and toxic potencies of these CDI systems, both yielded similar competitive advantages against cells lacking immunity. This can be explained by the fact that the less expressed system ( ) delivers a more potent toxin than the highly expressed system. Moreover, our results indicate that unlike most sequenced CDI bacterial isolates, the two loci of EC93 are located on a plasmid and are expressed in laboratory media.
ISSN:2057-5858
2057-5858
DOI:10.1099/mgen.0.000534