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Iron interferes with quorum sensing-mediated cooperation in Pseudomonas aeruginosa by affecting the expression of ppyR and mexT, in addition to rhlR
Feng Sun , Na Li , Lijia Wang , Huajun Feng , Dongsheng Shen , Meizhen Wang
J. Microbiol. 2020;58(11):938-944.   Published online October 30, 2020
DOI: https://doi.org/10.1007/s12275-020-0264-4
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AbstractAbstract
The stabilization of quorum sensing (QS) is vital for bacterial survival in various environments. Although the mechanisms of QS stabilization in certain conditions have been well studied, the impact of environmental factors has received much less attention. In this study, we show that the supplementation of 25 μM iron in competition experiments and 50 μM in evolution experiments to casein growth cultures significantly increased the possibility of population collapse by affecting elastase production. However, the expression of lasI and lasR remained constant regardless of iron concentration and hence this effect was not through interference with the LasIR circuit, which mainly regulates the secretion of elastase in Pseudomonas aeruginosa. However, the expression of rhlR was significantly inhibited by iron treatment, which could affect the production of elastase. Further, based on both reverse transcription quantitative polymerase chain reaction and gene knock-out assays, we show that iron inhibits the transcription of ppyR and enhances the expression of mexT, both of which decrease elastase production and correspondingly interfere with QS stabilization. Our findings show that environmental factors can affect the genes of QS circuits, interfering with QS stabilization. These findings are not only beneficial in understanding the mechanistic effect of iron on QS stabilization, but also demonstrate the complexity of QS stabilization by linking non-QS-related genes with QS traits.
Middle East respiratory syndrome coronavirus-encoded ORF8b strongly antagonizes IFN-β promoter activation: its implication for vaccine design
Jeong Yoon Lee , Sojung Bae , Jinjong Myoung
J. Microbiol. 2019;57(9):803-811.   Published online August 27, 2019
DOI: https://doi.org/10.1007/s12275-019-9272-7
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  • 38 Citations
AbstractAbstract
Middle East respiratory syndrome coronavirus (MERS-CoV) is a causative agent of severe-to-fatal pneumonia especially in patients with pre-existing conditions, such as smoking and chronic obstructive pulmonary disease (COPD). MERS-CoV transmission continues to be reported in the Saudi Arabian Peninsula since its discovery in 2012. However, it has rarely been epidemic outside the area except one large outbreak in South Korea in May 2015. The genome of the epidemic MERS-CoV isolated from a Korean patient revealed its homology to previously reported strains. MERS-CoV encodes 5 accessory proteins and generally, they do not participate in the genome transcription and replication but rather are involved in viral evasion of the host innate immune responses. Here we report that ORF8b, an accessory protein of MERSCoV, strongly inhibits both MDA5- and RIG-I-mediated activation of interferon beta promoter activity while downstream signaling molecules were left largely unaffected. Of note, MDA5 protein levels were significantly down-regulated by ORF8b and co-expression of ORF4a and ORF4b. These novel findings will facilitate elucidation of mechanisms of virus-encoded evasion strategies, thus helping design rationale antiviral countermeasures against deadly MERS-CoV infection.

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