The human pathogen Vibrio cholerae is a highly motile organism by virtue of a polar flagellum, and motility has been inferred to be an important aspect of virulence. It has previously been demonstrated that the sigma(54)-dependent activator FlrC is necessary for both flagellar synthesis and for enhanced intestinal colonization. In order to characterize FlrC binding, we analyzed two FlrC-dependent promoters, the highly transcribed flaA promoter and the weakly transcribed flgK promoter, utilizing transcriptional lacZ fusions, mobility shift assays, and DNase I footprinting. Promoter fusion studies showed that the smallest fragment with wild-type transcriptional activity for flaAp was from positions -54 to +137 with respect to the start site, and from -63 to +144 for flgKp. Gel mobility shift assays indicated that FlrC binds to a fragment containing the region from positions +24 to +95 in the flaAp, and DNase I footprinting identified a protected region between positions +24 and +85. Mobility shift and DNase I footprinting indicated weak binding of FlrC to a region downstream of the flgKp transcription start site. These results demonstrate a relatively novel sigma(54)-dependent promoter architecture, with the activator FlrC binding downstream of the sigma(54)-dependent transcription start sites. When the FlrC binding site(s) in the flaA promoter was moved a large distance (285 bp) upstream of the transcription start site of either flaAp or flgKp, high levels of FlrC-dependent transcription resulted, indicating that this binding region functions as an enhancer element. In contrast, the relatively weak FlrC binding site(s) in the flgK promoter failed to function as an enhancer element at either promoter, suggesting that FlrC binding strength contributes to enhancer activity. Our results suggest that the differences in FlrC binding to various flagellar promoters results in the differences in transcription levels that mirror the relative requirement for the flagellar components within the flagellum.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1082837PMC
http://dx.doi.org/10.1128/JB.187.9.3158-3170.2005DOI Listing

Publication Analysis

Top Keywords

flrc binding
24
mobility shift
12
dnase footprinting
12
start site
12
transcription start
12
flrc
10
binding
9
vibrio cholerae
8
activator flrc
8
flaa promoter
8

Similar Publications

Phosphorylation of the σ-dependent transcription activator FlrC by the sensor histidine kinase FlrB is essential for flagellar synthesis of Vibrio cholerae. Despite that, the structure, sensory signal, and mechanistic basis of function of FlrB were elusive. Here, we report the crystal structure of the sensory PAS domain of FlrB in its functional dimeric state that exhibits a unique architecture.

View Article and Find Full Text PDF

If left unrepaired, the major oxidative DNA lesion 7,8-dihydro-8-oxoguanine (oxoG) promotes G-to-T transversions by favorably adopting a syn conformation and base pairing with dATP during replication. The human oxoG DNA glycosylase hOGG1 senses and removes oxoG amid millions-fold excess of guanine, thereby counteracting the genotoxic effects of the major oxidative damage. Crystal structures of hOGG1 in complex with oxoG-containing DNA have provided key insights into the lesion recognition and catalysis mechanisms of the enzyme.

View Article and Find Full Text PDF

ToxR modulates biofilm formation in fish pathogen Vibrio harveyi.

Lett Appl Microbiol

February 2022

Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, China.

Vibrio harveyi is a common aquaculture pathogen causing diseases in a variety of aquatic animals. toxR, a conserved virulence-associated gene in vibrios, is identified in V. harveyi 345, a pathogenic strain isolated from diseased fish.

View Article and Find Full Text PDF

Regulatory Effects of CsrA in Vibrio cholerae.

mBio

February 2021

Department of Molecular Biosciences and LaMontagne Center for Infectious Diseases, The University of Texas at Austin, Austin, Texas, USA

CsrA is a posttranscriptional global regulator in Although CsrA is critical for survival within the mammalian host, the regulatory targets of CsrA remain mostly unknown. To identify pathways controlled by CsrA, RNA-seq transcriptome analysis was carried out by comparing the wild type and the mutant grown to early exponential, mid-exponential, and stationary phases of growth. This enabled us to identify the global effects of CsrA-mediated regulation throughout the growth cycle.

View Article and Find Full Text PDF

The bacterial enhancer-binding protein (bEBP) FlrC, controls motility and colonization of by regulating the transcription of class-III flagellar genes in σ-dependent manner. However, the mechanism by which FlrC regulates transcription is not fully elucidated. Although, most bEBPs require nucleotides to stimulate the oligomerization necessary for function, our previous study showed that the central domain of FlrC (FlrC) forms heptamer in a nucleotide-independent manner.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!