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Type II toxin/antitoxin system ParE SO /CopA SO stabilizes prophage CP4So in Shewanella oneidensis

Jianyun Yao; Yunxue Guo; Pengxia Wang; Zhenshun Zeng; Baiyuan Li; Kaihao Tang; Xiaoxiao Liu; Xiaoxue Wang
Environmental Microbiology · Vol. 20, Issue 3 · pp. 1224-1239 · 2018

Abstract

Summary Toxin/antitoxin (TA) loci are commonly found in mobile genetic elements such as plasmids and prophages. However, the physiological functions of these TA loci in prophages and cross‐regulation among these TA loci remain largely unexplored. Here, we characterized a newly discovered type II TA pair, ParE SO /CopA SO , in the CP4So prophage in Shewanella oneidensis . We demonstrated that ParE SO /CopA SO plays a critical role in the maintenance of CP4So in host cells after its excision. The toxin ParE SO inhibited cell growth, resulting in filamentous growth and eventually cell death. The antitoxin CopA SO neutralized the toxicity of ParE SO through direct protein‐protein interactions and repressed transcription of the TA operon by binding to a DNA motif in the promoter region containing two inverted repeats [5′‐ GTA N TAC (N) 3 GTA N TAC ‐3′]. CopA SO also repressed transcription of another TA system PemK SO / PemI SO in megaplasmid pMR‐1 of S. oneidensis through binding to a highly similar DNA motif in its promoter region. CopA SO homologs are widely spread in Shewanella and other Proteobacteria , either as a component of a TA pair or as orphan antitoxins. Our study thus illustrated the cross‐regulation of the TA systems in different mobile genetic elements and expanded our understanding of the physiological function of TA systems.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2018-03-01
Publication Year2018
Volume20
Issue3
Pages1224-1239
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.14068
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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