Type I Toxin-Antitoxin Loci: hok/sok and fst

Chapter

Abstract

The first type I TA locus to be discovered was hok/sok of plasmid R1 due to its ability to stabilize heterologous replicons in Escherichia coli. The unraveling of the mechanism of plasmid stabilization yielded a surprise: hok/sok increases plasmid maintenance by killing of plasmid-free cells, a mechanism known as post-segregational killing (PSK). The hok/sok locus codes for two RNAs: Sok antisense RNA that inhibits translation of the toxin-encoding hok mRNA. The system is regulated such that hok mRNA is translated in plasmid-free cells only. Initially, it was difficult to understand how a cis-acting antisense (Sok-RNA) that is fully complementary to its target RNA (hok mRNA) apparently could regulate translation of the mRNA in a reversible manner. The elucidation of the underlying mechanism behind the paradox revealed a unique type of gene regulation that involves mRNA processing and refolding. The par locus of plasmid pAD1 from Enterococcus faecalis also stabilizes plasmids by PSK and also encodes two RNAs that interact. However, the mechanism by which the mRNA (RNA I) avoids irreversible inactivation by the antisense RNA (RNA II) is entirely different from that of hok/sok. Surprisingly, the chromosome of E. coli K-12 encodes type I TA loci called ldr that appears to share properties with both hok/sok and par of pAD1. This chapter reviews the hok/sok, par, and ldr loci.

Keywords

Peptide Toxin Cell Wall Growth Intramolecular Structure Plasmid pAD1 Bulky Hydrophobic Amino Acid 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer-Verlag Berlin Heidelberg 2013

Authors and Affiliations

  1. 1.Division of Basic Biomedical SciencesSanford School of MedicineVermillionUSA

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