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A toxin-antitoxin system is a set of two or more closely linked genes that together encode both a protein 'poison' and a corresponding 'antidote'. When these systems are contained on plasmids – transferable genetic elements – they ensure that only the daughter cells that inherit the plasmid survive after cell division. If the plasmid is absent in a daughter cell, the unstable anti-toxin is degraded and the stable toxic protein kills the new cell; this is known as 'post-segregational killing' (PSK). Toxin-antitoxin systems are widely distributed in prokaryotes, and organisms often have them in multiple copies. Toxin-antitoxin systems are typically classified according to how the antitoxin neutralises the toxin. In a type I toxin-antitoxin system, the translation of messenger RNA (mRNA) that encodes the toxin is inhibited by the binding of a small non-coding RNA antitoxin to the mRNA. The protein toxin in a type II system is inhibited post-translationally by the binding of another protein antitoxin. A single example of a type III toxin-antitoxin system has been described whereby a protein toxin is bound directly by an RNA molecule. Toxin-antitoxin genes are often transferred through horizontal gene transfer and are associated with pathogenic bacteria, having been found on plasmids conferring antibiotic resistance and virulence.〔 Chromosomal toxin-antitoxin systems also exist, some of which perform cell functions such as responding to stresses, causing cell cycle arrest and bringing about programmed cell death.〔 In evolutionary terms, toxin-antitoxin systems can be considered selfish DNA in that the purpose of the systems are to replicate, regardless of whether they benefit the host organism or not. Some have proposed adaptive theories to explain the evolution of toxin-antitoxin systems; for example, chromosomal toxin-antitoxin systems could have evolved to prevent the inheritance of large deletions of the host genome. Toxin-antitoxin systems have several biotechnological applications, such as a method of maintaining plasmids in cell lines, targets for antibiotics, and as positive selection vectors. ==Evolutionary advantage== Plasmid stabilising toxin-antitoxin systems have been used as examples of selfish DNA as part of the gene centered view of evolution. It has been theorised that toxin-antitoxin loci serve only to maintain their own DNA, at the expense of the host organism.〔 Other theories propose the systems have evolved to increase the fitness of plasmids in competition with other plasmids. Thus, the toxin-antitoxin system confers an advantage to the host DNA by eliminating competing plasmids in cell progeny. This theory was corroborated through computer modelling. This does not, however, explain the presence of toxin-antitoxin systems on chromosomes. Chromosomal toxin-antitoxin systems have a number of adaptive theories explaining their success at natural selection. The simplest explanation of their existence on chromosomes is that they prevent harmful large deletions of the cell's genome, though arguably deletions of large coding regions are fatal to a daughter cell regardless.〔 ''MazEF'', a toxin-antitoxin locus found in ''E. coli'' and other bacteria, induces programmed cell death in response to starvation, specifically a lack of amino acids. This releases the cell's contents for absorption by neighbouring cells, potentially preventing the death of close relatives, and thereby increasing the inclusive fitness of the cell that perished. This is an example of altruism and how bacterial colonies resemble multicellular organisms.〔 Another theory states that chromosomal toxin-antitoxin systems are designed to be bacteriostatic rather than bactericidal.〔 RelE, for example, is a global inhibitor of translation during nutrient stress, and its expression reduces the chance of starvation by lowering the cell's nutrient requirements. A homologue of mazF toxin called mazF-mx is essential for fruiting body formation in ''Myxococcus xanthus''. When nutrients become limiting in this swarming bacteria, a group of 50,000 cells converge into a fruiting body structure. The maxF-mx toxin is a component of this nutrient-stress pathway; it enables a percentage of cells within the fruiting body to form myxospores. It has been suggested that ''M. xanthus'' has hijacked the toxin-antitoxin system, replacing the antitoxin with its own molecular control to regulate its development.〔 It has also been proposed that chromosomal copies of plasmid toxin-antitoxin systems may serve as anti-addiction modules – a method of omitting a plasmid from progeny without suffering the effects of the toxin. An example of this is an antitoxin on the ''Erwinia chrysanthemi'' genome that counteracts the toxic activity of an F plasmid toxin counterpart. Nine possible functions of toxin-antitoxin systems have been proposed. These are: # Junk – they have been acquired from plasmids and retained due to their addictive nature. # Stabilisation of genomic parasites – chromosomal remnants from transposons and bacteriophages. # Selfish alleles – non-addictive alleles are unable to replace addictive alleles during recombination but the opposite is able to occur. # Gene regulation – some toxins act as a means of general repression of gene expression while others are more specific. # Growth control – bacteriostatic toxins, as mentioned above, restrict growth rather than killing the host cell.〔 # Persisters – some bacterial populations contain a sub-population of 'persisters' controlled by toxin-antitoxin systems that are slow-growing, hardy individuals, which potentially insure the population against catastrophic loss. # Programmed cell arrest and the preservation of the commons – the altruistic explanation as demonstrated by ''MazEF'', detailed above. # Programmed cell death – similar to the above function, although individuals must have variable stress survival level to prevent entire population destruction. # Antiphage mechanism – when bacteriophage interrupt the host cell's transcription and translation, a toxin-antitoxin system may be activated that limits the phage's replication. An experiment where five TA systems were deleted from a strain of ''E. coli'' found no evidence that the TA systems conferred an advantage to the host. This result casts doubt on the growth control and programmed cell death hypotheses. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Toxin-antitoxin system」の詳細全文を読む スポンサード リンク
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