Desferrioxamine-dependent iron transport in Erwinia amylovora CFBP1430: cloning of the gene encoding the ferrioxamine receptor FoxR

BioMetals ◽  
1996 ◽  
Vol 9 (2) ◽  
Author(s):  
R�my Kachadourian ◽  
Alia Dellagi ◽  
Jacqueline Laurent ◽  
Laurent Bricard ◽  
Gerhard Kunesch ◽  
...  
Keyword(s):  
Iron Transport ◽  
Erwinia Amylovora ◽  
Gene Encoding ◽  
Ferrioxamine Receptor

scholarly journals Expression of the Ferrioxamine Receptor Gene of Erwinia amylovora CFBP 1430 During Pathogenesis

1999 ◽  
Vol 12 (5) ◽  
pp. 463-466 ◽  
Author(s):  
Alia Dellagi ◽  
Danièle Reis ◽  
Brigitte Vian ◽  
Dominique Expert
Keyword(s):  
Transport System ◽  
Iron Transport ◽  
Erwinia Amylovora ◽  
Receptor Gene ◽  
Bacterial Cells ◽  
In Planta ◽  
Disease Evolution ◽  
Lacz Activity ◽  
Leaf Tissues ◽  
Ferrioxamine Receptor

Mutants of Erwinia amylovora CFBP 1430 lacking a functional high-affinity iron transport system mediated by desferrioxamine are impaired in their ability to initiate fire blight symptoms (A. Dellagi, M.-N. Brisset, J.-P. Paulin, and D. Expert. Mol. Plant-Microbe Interact. 11:734–742, 1998). In this study, a chromosomal transcriptional lacZ fusion was used to analyze the expression in planta of the E. amylovora ferrioxamine receptor gene foxR. LacZ activity produced by the strain harboring the fusion was highly induced in iron-restricted conditions and in inoculated apple leaf tissues. Microscopic observation revealed differential expression of this gene in relation to the localization and density of bacterial cells within the diseased tissue. Thus, the ability of bacterial cells to express their iron transport system in accordance with environmental conditions is likely important for disease evolution.

scholarly journals Identification and Characterization of theErwinia amylovora rpoS Gene: RpoS Is Not Involved in Induction of Fireblight Disease Symptoms

1998 ◽  
Vol 180 (24) ◽  
pp. 6789-6792 ◽  
Author(s):  
M. Anderson ◽  
C. E. Pollitt ◽  
I. S. Roberts ◽  
J. A. Eastgate
Keyword(s):  
Sigma Factor ◽  
Erwinia Amylovora ◽  
Environmental Stresses ◽  
Alternative Sigma Factor ◽  
Gene Encoding ◽  
Disease Symptoms ◽  
Highly Sensitive ◽  
Identification And Characterization ◽  
Sigma Factor Rpos

ABSTRACT The Erwinia amylovora rpoS gene, encoding the alternative sigma factor RpoS, has been cloned and characterized. Though highly sensitive to a number of environmental stresses, anE. amylovora rpoS mutant was not compromised in its ability to grow or cause disease symptoms within apple seedlings or in an overwintering model.

scholarly journals Contribution of metal transporters of the ABC, ZIP, and NRAMP families to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis

2021 ◽  
Author(s):  
Tanya Puccio ◽  
Karina Kunka ◽  
Todd Kitten
Keyword(s):  
Infective Endocarditis ◽  
Iron Transport ◽  
Rabbit Model ◽  
Gene Encoding ◽  
Metal Transporters ◽  
Streptococcus Sanguinis ◽  
Manganese Uptake ◽  
Zip Family ◽  
Family Protein

Streptococcus sanguinis is an important cause of infective endocarditis. In strain SK36, the ABC-family manganese transporter, SsaACB, is essential for virulence. We have now identified a ZIP-family protein, TmpA, as a secondary manganese transporter. A tmpA mutant had no phenotype, but a ΔssaACB ΔtmpA mutant was far more attenuated for serum growth and somewhat more attenuated for virulence in a rabbit model than its ΔssaACB parent. The growth of both mutants was restored by supplemental manganese, but the ΔssaACB ΔtmpA mutant required twenty-fold more and accumulated less. Although ZIP-family proteins are known for zinc and iron transport, TmpA-mediated transport of either metal was minimal. In contrast to ssaACB and tmpA, which appear ubiquitous in S. sanguinis, a mntH gene encoding an NRAMP-family transporter has been identified in relatively few strains, including VMC66. As in SK36, deletion of ssaACB greatly diminished VMC66 endocarditis virulence and serum growth, and deletion of tmpA from this mutant diminished virulence further. Virulence was not significantly altered by deletion of mntH from either VMC66 or its ΔssaACB mutant. This and the accompanying paper together suggest that SsaACB is of primary importance for endocarditis virulence while secondary transporters TmpA and MntH contribute to growth under differing conditions.

B-Vitamins, Methylenetetrahydrofolate Reductase (MTHFR) and Hypertension

2011 ◽  
Vol 81 (4) ◽  
pp. 240-244 ◽  
Author(s):  
Mary Ward ◽  
Carol P Wilson ◽  
J J Strain ◽  
Geraldine Horigan ◽  
John M. Scott ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Low Dose ◽  
Methylenetetrahydrofolate Reductase ◽  
Genetic Determinant ◽  
Gene Encoding ◽  
Homocysteine Concentration ◽  
Homozygous Mutant ◽  
B Vitamin

Hypertension is a leading risk factor for cardiovascular disease (CVD) and stroke. A common polymorphism in the gene encoding the enzyme methylenetetrahydrofolate reductase (MTHFR), previously identified as the main genetic determinant of elevated homocysteine concentration and also recognized as a risk factor for CVD, appears to be independently associated with hypertension. The B-vitamin riboflavin is required as a cofactor by MTHFR and recent evidence suggests it may have a role in modulating blood pressure, specifically in those with the homozygous mutant MTHFR 677 TT genotype. If studies confirm that this genetic predisposition to hypertension is correctable by low-dose riboflavin, the findings could have important implications for the management of hypertension given that the frequency of this polymorphism ranges from 3 to 32 % worldwide.

Identification of a single-copy gene encoding a Type I chlorophyll a/b-binding polypeptide of photosystem I in Arabidopsis thaliana

1992 ◽  
Vol 84 (4) ◽  
pp. 561-567 ◽  
Author(s):  
Poul E. Jensen ◽  
Michael Kristensen ◽  
Tine Hoff ◽  
Jan Lehmbeck ◽  
Bjarne M. Stummann ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Chlorophyll A ◽  
Photosystem I ◽  
Single Copy ◽  
Type I ◽  
Single Copy Gene ◽  
Gene Encoding ◽  
Copy Gene

Characterisation of Type 2N von Willebrand Disease Using Phenotypic and Molecular Techniques

1996 ◽  
Vol 75 (06) ◽  
pp. 959-964 ◽  
Author(s):  
I M Nesbitt ◽  
A C Goodeve ◽  
A M Guilliatt ◽  
M Makris ◽  
F E Preston ◽  
...  
Keyword(s):  
Direct Sequencing ◽  
Von Willebrand Disease ◽  
Molecular Techniques ◽  
Haemophilia A ◽  
Binding Region ◽  
Gene Encoding ◽  
Covalently Linked ◽  
Von Willebrand ◽  
Willebrand Factor

Summaryvon Willebrand factor (vWF) is a multimeric glycoprotein found in plasma non covalently linked to factor VIII (FVIII). Type 2N von Willebrand disease (vWD) is caused by a mutation in the vWF gene that results in vWF with a normal multimeric pattern, but with reduced binding to FVIII.We have utilised methods for the phenotypic and genotypic detection of type 2N vWD. The binding of FVIII to vWF in 69 patients, 36 with type 1 vWD, 32 with mild haemophilia A and one possible haemophilia A carrier with low FVIII levels was studied. Of these, six were found to have reduced binding (five type 1 vWD, one possible haemophilia A carrier), DNA was extracted from these patients and exons 18-23 of the vWF gene encoding the FVIII binding region of vWF were analysed. After direct sequencing and chemical cleavage mismatch detection, a Thr28Met mutation was detected in two unrelated individuals, one of whom appears to be a compound heterozygote for the mutation and a null allele. No mutations were found in the region of the vWF gene encoding the FVIII binding region of vWF in the other four patients

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