Linked Life Data

9675889

Source:http://linkedlifedata.com/resource/pubmed/id/9675889

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1998-8-20
pubmed:databankReference
pubmed:abstractText
To investigate the role of iron in Erwinia amylovora pathogenicity, virulence properties of two mutants of strain CFBP 1430 isolated by insertional mutagenesis and affected in the iron transport pathway mediated by desferrioxamine (DFO) were analyzed. One mutation (dfoA::MudIIpR13) disrupts DFO biosynthesis. The present analysis shows that this mutation affects an open reading frame that belongs to a biosynthetic gene cluster and shares identity with the alcA gene required for synthesis of the siderophore alcaligin in Bordetella spp. A second mutation (foxR::MudIIpR13) affects the synthesis of the ferrioxamine receptor FoxR, encoded by the foxR gene, and was shown to be transcribed into a monocistronic message. Accordingly, the foxR mutant accumulates DFO in the external medium. The growth of the mutants when supplied with various iron sources was examined; it indicates that the production of DFO and the specific transport of the DFO ferric complex are required only when iron is strongly liganded. Pathogenicity was scored after inoculation of apple seedlings and after infection of apple flowers. On seedlings, the DFO biosynthetic mutant behaved like the wild-type strain while the frequency of necrotic plants caused by the receptor mutant decreased by a factor of two to five, depending on the initial inoculum. On flowers, both mutants were strongly affected in their ability to initiate a necrotic symptom and their growth was reduced by two orders of magnitude relative to the wild-type strain. However, the virulence of the dfoA mutant varied with the inoculum concentration. Unlike the foxR mutant, the dfoA mutant only weakly induced plant cell electrolyte leakage in tobacco leaf disks. The supply with exogenous DFO, only when iron free, restored the ability to induce electrolyte leakage to the dfoA mutant and increased the leakage induced by other strains. DFO alone was not an inducer. Iron-free DFO was able to protect E. amylovora cells against lethal doses of hydrogen peroxide. The main conclusion was that production of DFO in E. amylovora during pathogenesis is not only a critical function for iron acquisition, but can play a role in the oxidative burst elicited by the bacteria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0894-0282
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
734-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Dual role of desferrioxamine in Erwinia amylovora pathogenicity.
pubmed:affiliation
Laboratoire de Pathologie Végétale, INRA/INA P-G, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't