The requirement of chrysobactin dependent iron transport for virulence incited by Erwinia chrysanthemi on Saintpaulia ionantha

1991 ◽  
Vol 130 (1-2) ◽  
pp. 263-271 ◽  
Author(s):  
C. Enard ◽  
T. Franza ◽  
C. Neema ◽  
P. R. Gill ◽  
M. Persmark ◽  
...  
1999 ◽  
Vol 12 (2) ◽  
pp. 119-128 ◽  
Author(s):  
Thierry Franza ◽  
Christele Sauvage ◽  
Dominique Expert

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.


2002 ◽  
Vol 15 (11) ◽  
pp. 1181-1191 ◽  
Author(s):  
Thierry Franza ◽  
Isabelle Michaud-Soret ◽  
Pierrette Piquerel ◽  
Dominique Expert

Two major virulence determinants of the plant-pathogenic enterobacterium Erwinia chrysanthemi strain 3937 are the production of pectate lyase enzymes that degrade plant cell walls and expression of two high-affinity iron uptake systems mediated by two structurally unrelated siderophores, chrysobactin and achromobactin. Low iron availability is a signal that triggers transcription of the genes encoding pectate lyases PelD and PelE as well as that of genes involved in iron transport. This metalloregulation is mediated by the transcriptional repressor Fur. In this study, we analyzed the molecular mechanisms of this control. We purified the Erwinia chrysanthemi Fur protein. Band shift assays showed that Fur specifically binds in vitro to the regulatory regions of the genes encoding the ferrichrysobactin outer membrane receptor Fct and the pectate lyases PelD and PelE. We identified the Fur-binding sites of these promoter regions by performing DNase I footprinting experiments. From these data, we propose that Fur could inhibit the activation of the pelD and pelE genes by the cAMP receptor protein CRP according to an anti-activation mechanism. To identify other possible effectors involved in this control, we screened a bank of insertion mutants for an increase in transcriptional activity of pelD and fct genes in response to iron limitation. We isolated a mutant affected in the kdgK gene encoding the 2-keto-3-deoxygluconate (KDG) kinase, an enzyme involved in pectin catabolism. The growth of this mutant in the presence of pectic compounds led to a constitutive expression of iron transport genes as well as complete derepression of the pectinolysis genes. This effect was caused by intracellular accumulation of KDG. However, the derepression of iron transport genes by KDG does not involve the KdgR regulator of pectinolysis genes, which uses KDG as inducer. Thus, in Erwinia chrysanthemi, iron depletion or presence of KDG induces transcription of the genes involved in iron assimilation and pectinolysis. These important pathogenicity functions are coregulated by responding to common signals encountered in planta.


2007 ◽  
Vol 189 (19) ◽  
pp. 7053-7061 ◽  
Author(s):  
Aurélie Delangle ◽  
Anne-France Prouvost ◽  
Virginie Cogez ◽  
Jean-Pierre Bohin ◽  
Jean-Marie Lacroix ◽  
...  

ABSTRACT β-1,4-Galactan is a major component of the ramified regions of pectin. Analysis of the genome of the plant pathogenic bacteria Erwinia chrysanthemi revealed the presence of a cluster of eight genes encoding proteins potentially involved in galactan utilization. The predicted transport system would comprise a specific porin GanL and an ABC transporter made of four proteins, GanFGK2. Degradation of galactans would be catalyzed by the periplasmic 1,4-β-endogalactanase GanA, which released oligogalactans from trimer to hexamer. After their transport through the inner membrane, oligogalactans would be degraded into galactose by the cytoplasmic 1,4-β-exogalactanase GanB. Mutants affected for the porin or endogalactanase were unable to grow on galactans, but they grew on galactose and on a mixture of galactotriose, galactotetraose, galactopentaose, and galactohexaose. Mutants affected for the periplasmic galactan binding protein, the transporter ATPase, or the exogalactanase were only able to grow on galactose. Thus, the phenotypes of these mutants confirmed the functionality of the gan locus in transport and catabolism of galactans. These mutations did not affect the virulence of E. chrysanthemi on chicory leaves, potato tubers, or Saintpaulia ionantha, suggesting an accessory role of galactan utilization in the bacterial pathogeny.


2013 ◽  
Vol 1 (1) ◽  
pp. 49-53
Author(s):  
Julio César González Cárdenas ◽  
Pablo Elorza Martínez ◽  
Alejandra López Jiménez ◽  
Roberto Alejandro Mateos Rocha ◽  
Alfredo González Acosta

El presente trabajo tuvo como finalidad la identificación del agente causal de la Pudrición foliar blanda de la Violeta Africana en Tenango de las Flores, Huachinango, Puebla, México. Después de realizar los postulados de Koch, el agente causal fue identificado como Erwinia chrysanthemi. Este patógeno es considerado como el más importante de las enfermedades bacterianas en Violeta Africana debido a los niveles altos de daño que causa en las hojas. Los síntomas de la enfermedad incluyen lesiones blandas acuosas. Bajo condiciones favorables de clima, los síntomas de la enfermedad incluyen pudriciones blandas acuosas. La Reproducción Asexual es un factor importante de dispersión de la enfermedad, debido a que es un foco de infección para que la bacteria se reproduzca con mayor velocidad causando la muerte de las hojas y posteriormente de la planta.


1994 ◽  
Vol 176 (5) ◽  
pp. 1524-1526 ◽  
Author(s):  
M Boccara ◽  
J L Aymeric ◽  
C Camus

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