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.
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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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