HemN2 Regulates the Virulence of Pseudomonas donghuensis HYS through 7-Hydroxytropolone Synthesis and Oxidative Stress
Compared to pathogens and , HYS has stronger virulence towards . However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and viru...
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Published in | Biology (Basel, Switzerland) Vol. 13; no. 6; p. 373 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
24.05.2024
MDPI |
Subjects | |
Online Access | Get full text |
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Summary: | Compared to pathogens
and
,
HYS has stronger virulence towards
. However, the underlying mechanisms haven't been fully understood. The heme synthesis system is essential for
virulence, and former studies of HemN have focused on the synthesis of heme, while the relationship between HemN and
virulence were barely pursued. In this study, we hypothesized that
deficiency affected 7-hydroxytropolone (7-HT) biosynthesis and redox levels, thereby reducing bacterial virulence. There are four
genes in
HYS, and we reported for the first time that deletion of
significantly reduced the virulence of HYS towards
, whereas the reduction in virulence by the other three genes was not significant. Interestingly,
deletion significantly reduced colonization of
HYS in the gut of
. Further studies showed that HemN2 was regulated by GacS and participated in the virulence of
HYS towards
by mediating the synthesis of the virulence factor 7-HT. In addition, HemN2 and GacS regulated the virulence of
HYS by affecting antioxidant capacity and nitrative stress. In short, the findings that HemN2 was regulated by the Gac system and that it was involved in bacterial virulence via regulating 7-HT synthesis and redox levels were reported for the first time. These insights may enlighten further understanding of HemN-based virulence in the genus
. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 2079-7737 2079-7737 |
DOI: | 10.3390/biology13060373 |