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Iron regulation and pathogenicity in Erwinia chrysanthemi 3937: role of the Fur repressor protein.
Mol Plant Microbe Interact. 1999 Feb; 12(2):119-28.MP

Abstract

Low iron availability is a triggering signal for coordinated expression of the genes encoding pectate lyases PelB, PelC, PelD, and PelE, and chrysobactin iron transport functions, which are two main determinants of phytopathogenicity of the Erwinia chrysanthemi strain 3937. The possible implication of the ferric uptake regulation (Fur) protein in this process was investigated. The E. chrysanthemi fur gene was cloned by functional complementation of an Escherichia coli fur mutant and sequenced. The 444-bp open reading frame identified was found to code for a protein highly similar to the E. coli Fur regulator. An E. chrysanthemi fur null mutant was constructed by reverse genetics. This mutant showed altered growth capacity and reduced pathogenicity on African violets. In a fur background, transcriptional lacZ fusions to genes belonging to the E. chrysanthemi high affinity iron transport systems were constitutively expressed. Transcription of the pelA, pelD, and pelE genes was analyzed, using fusions to the uidA reporter gene. Iron availability and a fur mutation did not influence the expression of pelA. In the presence of iron, pelD and pelE transcription levels were higher in the fur mutant than in the parental strain. Furthermore, iron deficiency stimulated the expression of both fusions in the fur mutant. These findings indicate that, in E. chrysanthemi 3937, (i) Fur negatively controls iron transport and genes encoding PelD and PelE, and (ii) additional factor(s) mediate iron regulation of the pel genes.

Links

Publisher Full Text
apsjournals.apsnet.org
apsjournals.apsnet.org

Authors+Show Affiliations

Franza T
Laboratoire de Pathologie Végétale, INA P-G/INRA, Paris, France. franza@inapg.inra.fr
Sauvage C
No affiliation info available
Expert D
No affiliation info available

MeSH

Amino Acid SequenceBacterial ProteinsBase SequenceCloning, MolecularConsensus SequenceDickeya chrysanthemiEscherichia coliGene Expression Regulation, BacterialGenetic Complementation TestIronMolecular Sequence DataOpen Reading FramesPlant DiseasesPlantsPolysaccharide-LyasesPromoter Regions, GeneticRecombinant ProteinsRepressor ProteinsSequence AlignmentSequence Homology, Nucleic AcidTranscription, Genetic

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9926414

Citation

Franza, T, et al. "Iron Regulation and Pathogenicity in Erwinia Chrysanthemi 3937: Role of the Fur Repressor Protein." Molecular Plant-microbe Interactions : MPMI, vol. 12, no. 2, 1999, pp. 119-28.
Franza T, Sauvage C, Expert D. Iron regulation and pathogenicity in Erwinia chrysanthemi 3937: role of the Fur repressor protein. Mol Plant Microbe Interact. 1999;12(2):119-28.
Franza, T., Sauvage, C., & Expert, D. (1999). Iron regulation and pathogenicity in Erwinia chrysanthemi 3937: role of the Fur repressor protein. Molecular Plant-microbe Interactions : MPMI, 12(2), 119-28.
Franza T, Sauvage C, Expert D. Iron Regulation and Pathogenicity in Erwinia Chrysanthemi 3937: Role of the Fur Repressor Protein. Mol Plant Microbe Interact. 1999;12(2):119-28. PubMed PMID: 9926414.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Iron regulation and pathogenicity in Erwinia chrysanthemi 3937: role of the Fur repressor protein. AU - Franza,T, AU - Sauvage,C, AU - Expert,D, PY - 1999/2/2/pubmed PY - 1999/2/2/medline PY - 1999/2/2/entrez SP - 119 EP - 28 JF - Molecular plant-microbe interactions : MPMI JO - Mol Plant Microbe Interact VL - 12 IS - 2 N2 - Low iron availability is a triggering signal for coordinated expression of the genes encoding pectate lyases PelB, PelC, PelD, and PelE, and chrysobactin iron transport functions, which are two main determinants of phytopathogenicity of the Erwinia chrysanthemi strain 3937. The possible implication of the ferric uptake regulation (Fur) protein in this process was investigated. The E. chrysanthemi fur gene was cloned by functional complementation of an Escherichia coli fur mutant and sequenced. The 444-bp open reading frame identified was found to code for a protein highly similar to the E. coli Fur regulator. An E. chrysanthemi fur null mutant was constructed by reverse genetics. This mutant showed altered growth capacity and reduced pathogenicity on African violets. In a fur background, transcriptional lacZ fusions to genes belonging to the E. chrysanthemi high affinity iron transport systems were constitutively expressed. Transcription of the pelA, pelD, and pelE genes was analyzed, using fusions to the uidA reporter gene. Iron availability and a fur mutation did not influence the expression of pelA. In the presence of iron, pelD and pelE transcription levels were higher in the fur mutant than in the parental strain. Furthermore, iron deficiency stimulated the expression of both fusions in the fur mutant. These findings indicate that, in E. chrysanthemi 3937, (i) Fur negatively controls iron transport and genes encoding PelD and PelE, and (ii) additional factor(s) mediate iron regulation of the pel genes. SN - 0894-0282 UR - https://www.unboundmedicine.com/medline/citation/9926414/Iron_regulation_and_pathogenicity_in_Erwinia_chrysanthemi_3937:_role_of_the_Fur_repressor_protein_ L2 - https://apsjournals.apsnet.org/doi/10.1094/MPMI.1999.12.2.119?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -