Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress
<p>Abstract</p> <p>Background</p> <p>The global regulatory system ArcAB controls the anaerobic growth of <it>E. coli</it>, however, its role in aerobic conditions is not well characterized. We have previously reported that ArcA was necessary for <it>Sa...
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| Format: | Article |
| Language: | English |
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BMC
2009-08-01
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| Series: | BMC Microbiology |
| Online Access: | http://www.biomedcentral.com/1471-2180/9/183 |
| _version_ | 1818806467164110848 |
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| author | Lu Sangwei Chang Alexander C Loui Cindy |
| author_facet | Lu Sangwei Chang Alexander C Loui Cindy |
| author_sort | Lu Sangwei |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>The global regulatory system ArcAB controls the anaerobic growth of <it>E. coli</it>, however, its role in aerobic conditions is not well characterized. We have previously reported that ArcA was necessary for <it>Salmonella </it>to resist reactive oxygen species (ROS) in aerobic conditions.</p> <p>Results</p> <p>To investigate the mechanism of ROS resistance mediated by ArcAB, we generated deletion mutants of ArcA and ArcB in <it>E. coli</it>. Our results demonstrated that both ArcA and ArcB were necessary for resistance to hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), a type of ROS, and their function in this resistance was independent from H<sub>2</sub>O<sub>2 </sub>scavenge. Mutagenesis analysis of ArcA indicated that ROS resistance was mediated through a distinct signaling pathway from that used in anaerobic conditions. An abundant protein flagellin was elevated at both the protein and mRNA levels in the <it>ΔarcA </it>mutant as compared to the wild type <it>E. coli</it>, and deletion of flagellin restored the resistance of the <it>ΔarcA </it>mutant to H<sub>2</sub>O<sub>2</sub>. The resistance of the <it>ΔarcA </it>mutant <it>E. coli </it>to H<sub>2</sub>O<sub>2 </sub>can also be restored by amino acid supplementation, suggesting that a deficiency in amino acid and/or protein synthesis in the mutant contributed to its susceptibility to H<sub>2</sub>O<sub>2</sub>, which is consistent with the notion that protein synthesis is necessary for ROS resistance.</p> <p>Conclusion</p> <p>Our results suggest that in addition to its role as a global regulator for anaerobic growth of bacteria, ArcAB system is also important for bacterial resistance to ROS in aerobic conditions, possibly through its influence on bacterial metabolism, especially amino acid and/or protein assimilation and synthesis.</p> |
| first_indexed | 2024-12-18T19:10:14Z |
| format | Article |
| id | doaj.art-85237ffd24674cfca6c7e99a2e1e076e |
| institution | Directory Open Access Journal |
| issn | 1471-2180 |
| language | English |
| last_indexed | 2024-12-18T19:10:14Z |
| publishDate | 2009-08-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Microbiology |
| spelling | doaj.art-85237ffd24674cfca6c7e99a2e1e076e2022-12-21T20:56:17ZengBMCBMC Microbiology1471-21802009-08-019118310.1186/1471-2180-9-183Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stressLu SangweiChang Alexander CLoui Cindy<p>Abstract</p> <p>Background</p> <p>The global regulatory system ArcAB controls the anaerobic growth of <it>E. coli</it>, however, its role in aerobic conditions is not well characterized. We have previously reported that ArcA was necessary for <it>Salmonella </it>to resist reactive oxygen species (ROS) in aerobic conditions.</p> <p>Results</p> <p>To investigate the mechanism of ROS resistance mediated by ArcAB, we generated deletion mutants of ArcA and ArcB in <it>E. coli</it>. Our results demonstrated that both ArcA and ArcB were necessary for resistance to hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), a type of ROS, and their function in this resistance was independent from H<sub>2</sub>O<sub>2 </sub>scavenge. Mutagenesis analysis of ArcA indicated that ROS resistance was mediated through a distinct signaling pathway from that used in anaerobic conditions. An abundant protein flagellin was elevated at both the protein and mRNA levels in the <it>ΔarcA </it>mutant as compared to the wild type <it>E. coli</it>, and deletion of flagellin restored the resistance of the <it>ΔarcA </it>mutant to H<sub>2</sub>O<sub>2</sub>. The resistance of the <it>ΔarcA </it>mutant <it>E. coli </it>to H<sub>2</sub>O<sub>2 </sub>can also be restored by amino acid supplementation, suggesting that a deficiency in amino acid and/or protein synthesis in the mutant contributed to its susceptibility to H<sub>2</sub>O<sub>2</sub>, which is consistent with the notion that protein synthesis is necessary for ROS resistance.</p> <p>Conclusion</p> <p>Our results suggest that in addition to its role as a global regulator for anaerobic growth of bacteria, ArcAB system is also important for bacterial resistance to ROS in aerobic conditions, possibly through its influence on bacterial metabolism, especially amino acid and/or protein assimilation and synthesis.</p>http://www.biomedcentral.com/1471-2180/9/183 |
| spellingShingle | Lu Sangwei Chang Alexander C Loui Cindy Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress BMC Microbiology |
| title | Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress |
| title_full | Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress |
| title_fullStr | Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress |
| title_full_unstemmed | Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress |
| title_short | Role of the ArcAB two-component system in the resistance of <it>Escherichia coli </it>to reactive oxygen stress |
| title_sort | role of the arcab two component system in the resistance of it escherichia coli it to reactive oxygen stress |
| url | http://www.biomedcentral.com/1471-2180/9/183 |
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