Edwardsiella tarda the etiological agent for edwardsiellosis, a devastating fish disease prevailing in worldwide aquaculture industries was subjected to a molecular genetic study. To research into the influence when RpoN (σ(54) ) and RpoS (σ(38) ) were deleted simultaneously, the double deletion mutant of RpoN (σ(54) ) and RpoS (σ(38) ), namely rnrs, was constructed. Firstly, RpoN and RpoS are both essential for H2 O2 , starvation, high osmotic pressure and acid resistance, which have synergistic effect. Secondly, virulence of rnrs reduces significantly compared to E. tarda EIB 202 WT, ΔrpoN mutant and ΔrpoS mutant. Furthermore, transcriptional control of rpoS by rpoN in stationary phase was observed through qRT-PCR, while rpoS had no influence on rpoN in the level of transcription. Meanwhile, regulation of flagellar sigma factor σ(F) (FliA) and other flagella-related genes including flgA, flgK, flgL, motA, and motB by rpoS, and rpoN was found. fliA and other flagella-related genes were controlled positively by rpoN, while negatively by rpoS. At last, two differential expression genes in transcriptional level of rnrs strain were detected by DD-RT-PCR, namely cheY and narK. This study therefore indicated interaction between sigma factors RpoN and RpoS, which modulates stress response, virulence, motility, and provides new insights into the regulatory networks of E. tarda.
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http://dx.doi.org/10.1002/jobm.201300622 | DOI Listing |
mBio
January 2025
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
In , the causative agent of Lyme disease, differential gene expression is primarily governed by the alternative sigma factor RpoS (σ). Understanding the regulation of RpoS is crucial for elucidating how is maintained throughout its enzootic cycle. Our recent studies have shown that the homolog of Fur/PerR repressor/activator BosR functions as an RNA-binding protein that controls the mRNA stability.
View Article and Find Full Text PDFPLoS Pathog
December 2024
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Borrelia (or Borreliella) burgdorferi, the causative agent of Lyme disease, is a motile and invasive zoonotic pathogen adept at navigating between its arthropod vector and mammalian host. While motility and chemotaxis are well known to be essential for its enzootic cycle, the role of each methyl-accepting chemotaxis proteins (MCPs) in the infectious cycle of B. burgdorferi remains unclear.
View Article and Find Full Text PDFBMC Biol
November 2024
School of Resources and Environmental Engineering, Jiangsu University of Technology, 1801 Zhongwu Avenue, Changzhou, 213001, China.
NorR, as a single-target regulator, has been demonstrated to be involved in NO detoxification in bacteria under anaerobic conditions. Here, the norR gene was identified and deleted in the genome of Vibrio alginolyticus. The results showed that deletion of norR in Vibrio alginolyticus led to lower swarming motility and more biofilm formation on aerobic condition.
View Article and Find Full Text PDFbioRxiv
September 2024
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202.
In , the Lyme disease pathogen, differential gene expression is primarily controlled by the alternative sigma factor RpoS (σ). Understanding how RpoS levels are regulated is crucial for elucidating how is maintained throughout its enzootic cycle. Our recent studies have shown that a homolog of Fur/PerR repressor/activator, BosR, functions as an RNA-binding protein that controls the mRNA stability.
View Article and Find Full Text PDFInfect Immun
October 2024
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Lyme disease, the leading vector-borne disease in the United States and Europe, develops after infection with bacteria. Transmission of the spirochete from the tick vector to a vertebrate host requires global changes in gene expression that are controlled, in part, by the Rrp2/RpoN/RpoS alternative sigma factor cascade. Transcriptional studies defining the RpoS regulon have suggested that RpoS activates the transcription of paralogous family 52 (PFam52) genes.
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