Abstract
One of the simplest classes of genes involved in programmed death is that containing the toxin–antitoxin (TA) systems of prokaryotes. These systems are composed of an intracellular toxin and an antitoxin that neutralizes its effect. These systems, now classified into five types, were initially discovered because some of them allow the stable maintenance of mobile genetic elements in a microbial population through postsegregational killing or the death of cells that have lost these systems. Here, we demonstrate parallels between some TA systems and restriction–modification systems (RM systems). RM systems are composed of a restriction enzyme (toxin) and a modification enzyme (antitoxin) and limit the genetic flux between lineages with different epigenetic identities, as defined by sequence-specific DNA methylation. The similarities between these systems include their postsegregational killing and their effects on global gene expression. Both require the finely regulated expression of a toxin and antitoxin. The antitoxin (modification enzyme) or linked protein may act as a transcriptional regulator. A regulatory antisense RNA recently identified in an RM system can be compared with those RNAs in TA systems. This review is intended to generalize the concept of TA systems in studies of stress responses, programmed death, genetic conflict and epigenetics.
Highlights
The term ‘programmed death’ is usually associated with multicellular organisms
Programmed cell death induced by the segregational loss of a genetic element from a cell is called ‘postsegregational killing’ or ‘genetic addiction’
In this review, we primarily limit our discussion to typical Type II RM systems, calling them ‘RM systems’, unless otherwise stated. These RM systems act like type IV TA systems, where the modification enzyme activity prevents the cleavage of its target by the restriction enzyme
Summary
The term ‘programmed death’ is usually associated with multicellular organisms. Under certain conditions, an internal signal induces the death of individual cells as a ‘sacrifice’ to maintain the well-being of the entire organism. These RM systems act like type IV TA systems, where the modification enzyme (antitoxin) activity prevents the cleavage of its target by the restriction enzyme (toxin). In type II TA systems, such as Kid–Kis and MazF–MazE, the direct binding of the antitoxin to specific domains of the protein toxin, forming an oligomeric complex, inhibits the toxin activity [109].
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