Toxin-Antitoxin Systems in Pathogenic Bacteria
Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential...
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MDPI - Multidisciplinary Digital Publishing Institute
2022
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| Linkit: | ONIX_20220111_9783036506746_180 |
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| description | Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens. |
| format | Online |
| id | doab-20.500.12854ir-76444 |
| institution | Directory of Open Access Books |
| language | eng |
| publishDate | 2022 |
| publishDateRange | 2022 |
| publishDateSort | 2022 |
| publisher | MDPI - Multidisciplinary Digital Publishing Institute |
| publisherStr | MDPI - Multidisciplinary Digital Publishing Institute |
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| spelling | doab-20.500.12854ir-764442024-03-30T23:22:52Z Toxin-Antitoxin Systems in Pathogenic Bacteria Alonso, Juan Carlos tuberculosis toxin-antitoxin systems bacterial cell death NAD+ stress-response toxin–antitoxin system mazF type II toxin mRNA interferase X-ray crystallography cognate interactions cross-interactions molecular insulation antitoxin TA systems addiction anti-addiction type I toxin–antitoxin system small protein toxin structure Fst/Ldr family toxin–antitoxin M. tuberculosis bacteria pathogenesis protein–protein interactions cross-talk protein interface tolerance persistence cross-resistance toxin-antitoxin system PemI/PemK Klebsiella pneumoniae toxin–antitoxin systems toxin activation antibacterial agents bacterial persistence Stenotrophomonas maltophilia opportunistic pathogen clinical origin environmental origin biofilm antibiotic resistance cell wall inhibition nucleotide hydrolysis uridine diphosphate-N-acetylglucosamine n/a thema EDItEUR::M Medicine and Nursing Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens. 2022-01-11T13:32:08Z 2022-01-11T13:32:08Z 2021 book ONIX_20220111_9783036506746_180 9783036506746 9783036506753 https://directory.doabooks.org/handle/20.500.12854/76444 eng image/jpeg Attribution 4.0 International https://mdpi.com/books/pdfview/book/3879 https://mdpi.com/books/pdfview/book/3879 MDPI - Multidisciplinary Digital Publishing Institute 10.3390/books978-3-0365-0675-3 10.3390/books978-3-0365-0675-3 46cabcaa-dd94-4bfe-87b4-55023c1b36d0 9783036506746 9783036506753 170 Basel, Switzerland open access |
| spellingShingle | tuberculosis toxin-antitoxin systems bacterial cell death NAD+ stress-response toxin–antitoxin system mazF type II toxin mRNA interferase X-ray crystallography cognate interactions cross-interactions molecular insulation antitoxin TA systems addiction anti-addiction type I toxin–antitoxin system small protein toxin structure Fst/Ldr family toxin–antitoxin M. tuberculosis bacteria pathogenesis protein–protein interactions cross-talk protein interface tolerance persistence cross-resistance toxin-antitoxin system PemI/PemK Klebsiella pneumoniae toxin–antitoxin systems toxin activation antibacterial agents bacterial persistence Stenotrophomonas maltophilia opportunistic pathogen clinical origin environmental origin biofilm antibiotic resistance cell wall inhibition nucleotide hydrolysis uridine diphosphate-N-acetylglucosamine n/a thema EDItEUR::M Medicine and Nursing Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title | Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title_full | Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title_fullStr | Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title_full_unstemmed | Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title_short | Toxin-Antitoxin Systems in Pathogenic Bacteria |
| title_sort | toxin antitoxin systems in pathogenic bacteria |
| topic | tuberculosis toxin-antitoxin systems bacterial cell death NAD+ stress-response toxin–antitoxin system mazF type II toxin mRNA interferase X-ray crystallography cognate interactions cross-interactions molecular insulation antitoxin TA systems addiction anti-addiction type I toxin–antitoxin system small protein toxin structure Fst/Ldr family toxin–antitoxin M. tuberculosis bacteria pathogenesis protein–protein interactions cross-talk protein interface tolerance persistence cross-resistance toxin-antitoxin system PemI/PemK Klebsiella pneumoniae toxin–antitoxin systems toxin activation antibacterial agents bacterial persistence Stenotrophomonas maltophilia opportunistic pathogen clinical origin environmental origin biofilm antibiotic resistance cell wall inhibition nucleotide hydrolysis uridine diphosphate-N-acetylglucosamine n/a thema EDItEUR::M Medicine and Nursing |
| topic_facet | tuberculosis toxin-antitoxin systems bacterial cell death NAD+ stress-response toxin–antitoxin system mazF type II toxin mRNA interferase X-ray crystallography cognate interactions cross-interactions molecular insulation antitoxin TA systems addiction anti-addiction type I toxin–antitoxin system small protein toxin structure Fst/Ldr family toxin–antitoxin M. tuberculosis bacteria pathogenesis protein–protein interactions cross-talk protein interface tolerance persistence cross-resistance toxin-antitoxin system PemI/PemK Klebsiella pneumoniae toxin–antitoxin systems toxin activation antibacterial agents bacterial persistence Stenotrophomonas maltophilia opportunistic pathogen clinical origin environmental origin biofilm antibiotic resistance cell wall inhibition nucleotide hydrolysis uridine diphosphate-N-acetylglucosamine n/a thema EDItEUR::M Medicine and Nursing |
| url | ONIX_20220111_9783036506746_180 |