1887

Abstract

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.

Funding
This study was supported by the:
  • Stiftelsen för Strategisk Forskning
    • Principle Award Recipient: SannaKoskiniemi
  • Vetenskapsrådet
    • Principle Award Recipient: SannaKoskiniemi
  • National Institutes of Health (Award GM117373)
    • Principle Award Recipient: DavidA. Low
  • National Institutes of Health (Award GM117373)
    • Principle Award Recipient: ChristopherS. Hayes
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/content/journal/mgen/10.1099/mgen.0.000534
2021-03-01
2021-04-13
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