scholarly journals Cloning, sequencing, and transcriptional regulation of viuA, the gene encoding the ferric vibriobactin receptor of Vibrio cholerae.

1992 ◽  
Vol 174 (11) ◽  
pp. 3729-3738 ◽  
Author(s):  
J R Butterton ◽  
J A Stoebner ◽  
S M Payne ◽  
S B Calderwood
Yeast ◽  
1993 ◽  
Vol 9 (10) ◽  
pp. 1075-1084 ◽  
Author(s):  
Rajini Rao ◽  
Daniela Drummond-Barbosa ◽  
Carolyn W. Slayman

2000 ◽  
Vol 68 (3) ◽  
pp. 1400-1407 ◽  
Author(s):  
Phillip I. Tarr ◽  
Sima S. Bilge ◽  
James C. Vary ◽  
Srdjan Jelacic ◽  
Rebecca L. Habeeb ◽  
...  

ABSTRACT The mechanisms used by Shiga toxin (Stx)-producingEscherichia coli to adhere to epithelial cells are incompletely understood. Two cosmids from an E. coliO157:H7 DNA library contain an adherence-conferring chromosomal gene encoding a protein similar to iron-regulated gene A (IrgA) ofVibrio cholerae (M. B. Goldberg, S. A. Boyko, J. R. Butterton, J. A. Stoebner, S. M. Payne, and S. B. Calderwood, Mol. Microbiol. 6:2407–2418, 1992). We have termed the product of this gene the IrgA homologue adhesin (Iha), which is encoded by iha. Iha is 67 kDa in E. coliO157:H7 and 78 kDa in laboratory E. coli and is structurally unlike other known adhesins. DNA adjacent toiha contains tellurite resistance loci and is conserved in structure in distantly related pathogenic E. coli, but it is absent from nontoxigenic E. coli O55:H7, sorbitol-fermenting Stx-producing E. coli O157:H−, and laboratory E. coli. We have termed this region the tellurite resistance- and adherence-conferring island. We conclude that Iha is a novel bacterial adherence-conferring protein and is contained within an E. coli chromosomal island of conserved structure. Pathogenic E. coli O157:H7 has only recently acquired this island.


2017 ◽  
Vol 51 ◽  
pp. 10-16 ◽  
Author(s):  
Daniel M. da C. Leite ◽  
Livia C. Barbosa ◽  
Nathalia Mantuano ◽  
Carolina L. Goulart ◽  
Giovani C. Veríssimo da Costa ◽  
...  

1992 ◽  
Vol 174 (6) ◽  
pp. 1897-1903 ◽  
Author(s):  
C M Litwin ◽  
S A Boyko ◽  
S B Calderwood

2011 ◽  
Vol 193 (7) ◽  
pp. 1777-1782 ◽  
Author(s):  
A. Tan ◽  
J. Yang ◽  
M. Tauschek ◽  
J. Praszkier ◽  
R. M. Robins-Browne

2018 ◽  
Vol 200 (15) ◽  
Author(s):  
Nicolas L. Fernandez ◽  
Disha Srivastava ◽  
Amanda L. Ngouajio ◽  
Christopher M. Waters

ABSTRACT In Vibrio cholerae, high intracellular cyclic di-GMP (c-di-GMP) concentration are associated with a biofilm lifestyle, while low intracellular c-di-GMP concentrations are associated with a motile lifestyle. c-di-GMP also regulates other behaviors, such as acetoin production and type II secretion; however, the extent of phenotypes regulated by c-di-GMP is not fully understood. We recently determined that the sequence upstream of the DNA repair gene encoding 3-methyladenine glycosylase (tag) was positively induced by c-di-GMP, suggesting that this signaling system might impact DNA repair pathways. We identified a DNA region upstream of tag that is required for transcriptional induction by c-di-GMP. We further showed that c-di-GMP induction of tag expression was dependent on the c-di-GMP-dependent biofilm regulators VpsT and VpsR. In vitro binding assays and heterologous host expression studies show that VpsT acts directly at the tag promoter in response to c-di-GMP to induce tag expression. Last, we determined that strains with high c-di-GMP concentrations are more tolerant of the DNA-damaging agent methyl methanesulfonate. Our results indicate that the regulatory network of c-di-GMP in V. cholerae extends beyond biofilm formation and motility to regulate DNA repair through the VpsR/VpsT c-di-GMP-dependent cascade. IMPORTANCE Vibrio cholerae is a prominent human pathogen that is currently causing a pandemic outbreak in Haiti, Yemen, and Ethiopia. The second messenger molecule cyclic di-GMP (c-di-GMP) mediates the transitions in V. cholerae between a sessile biofilm-forming state and a motile lifestyle, both of which are important during V. cholerae environmental persistence and human infections. Here, we report that in V. cholerae c-di-GMP also controls DNA repair. We elucidate the regulatory pathway by which c-di-GMP increases DNA repair, allowing this bacterium to tolerate high concentrations of mutagens at high intracellular levels of c-di-GMP. Our work suggests that DNA repair and biofilm formation may be linked in V. cholerae.


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