PMID:20440275

Citation	Kohanski, MA, Dwyer, DJ and Collins, JJ (2010) How antibiotics kill bacteria: from targets to networks.Nat. Rev. Microbiol. 8:423-35
Abstract	Antibiotic drug-target interactions, and their respective direct effects, are generally well characterized. By contrast, the bacterial responses to antibiotic drug treatments that contribute to cell death are not as well understood and have proven to be complex as they involve many genetic and biochemical pathways. In this Review, we discuss the multilayered effects of drug-target interactions, including the essential cellular processes that are inhibited by bactericidal antibiotics and the associated cellular response mechanisms that contribute to killing. We also discuss new insights into these mechanisms that have been revealed through the study of biological networks, and describe how these insights, together with related developments in synthetic biology, could be exploited to create new antibacterial therapies.
Links	PubMed Online version:10.1038/nrmicro2333
Keywords	Anti-Bacterial Agents; Bacteria; Cell Wall; DNA Replication; Drug Discovery; Nucleic Acid Synthesis Inhibitors; Quinolones; RNA; Rifamycins
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Main Points of the Paper

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This review on antibiotic mechanisms argues that in many cases cell killing by antibiotics with diverse targets is due to a common indirect mechanism involving induction of oxidative stress leading to hydroxyl radical production. See Figure 2.

Materials and Methods Used

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Phenotype Annotations

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Species	Taxon ID	Strain	Gene (if known)	OMP	Phenotype	Details	Evidence	Notes
					Sensitivity to	Inhibition of DNA replication
					Sensitivity to	topoisomerase-catalysed DNA strand breakage
					Sensitivity to	Inhibition of RNA synthesis		rifampicin streptolydigin amanitin (eukaryotes)
					Sensitivity to	Inhibition of cell wall synthesis
					Sensitivity to	Inhibition of cell wall synthesis resulting in lysis
					Sensitivity to	Inhibition of protein synthesis
					Sensitivity to	Increased protein mistranslation
					Sensitivity to	Induction of hydroxyl radical production
					Sensitivity to	Loss of membrane potential		uncouplers pore-formers
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References

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