Flavohaemoglobin HmpX: a new pathogenicity determinant in Erwinia chrysanthemi strain 3937

Favey, Sylvie; Labesse, Gilles; Vouille, Véronique; Boccara, Martine

doi:10.1099/13500872-141-4-863

Cited by 70 publications

(68 citation statements)

References 35 publications

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“…Pseudomonas syringae pv tomato carrying the avirulence gene avrB were transformed with a pRK415 broad host vector (Keen et al, 1988) carrying the complete coding sequence of hmpX (Favey et al, 1995) under control of the Lac promoter, which is constitutively active in Pseudomonas. Detailed description of the construction of pRK415-hmpX and maintenance in Pseudomonas is not provided (M. Boccara, C. Mills, J. Zeier, C. Anzi, C. Lamb, R. Poole, and M. Delledonne, unpublished data).…”

Section: Growth Of Plant-pathogens and Infectionmentioning

confidence: 99%

“…We then compared the defense responses of NOdeficient plants and wild-type Arabidopsis following challenge with avirulent P. syringae pv tomato (Pst) bacteria. Additionally, we employed avirulent Pst expressing the hmpX gene from Erwinia chrysanthemi [Pst(avr-hmpX)] (Favey et al, 1995) that encodes a highly similar NOD to lower NO levels specifically at the side of pathogen infection. We then challenged wild-type Arabidopsis and hmp-expressing Arabidopsis plants with Pst(avr-hmpX) to study the effect of NO removal at both the plant and the pathogen side.…”

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Genetic Elucidation of Nitric Oxide Signaling in Incompatible Plant-Pathogen Interactions

et al. 2004

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Recent experiments indicate that nitric oxide (NO) plays a pivotal role in disease resistance and several other physiological processes in plants. However, most of the current information about the function of NO in plants is based on pharmacological studies, and additional approaches are therefore required to ascertain the role of NO as an important signaling molecule in plants. We have expressed a bacterial nitric oxide dioxygenase (NOD) in Arabidopsis plants and/or avirulent Pseudomonas syringae pv tomato to study incompatible plant-pathogen interactions impaired in NO signaling. NOD expression in transgenic Arabidopsis resulted in decreased NO levels in planta and attenuated a pathogen-induced NO burst. Moreover, NOD expression in plant cells had very similar effects on plant defenses compared to NOD expression in avirulent Pseudomonas. The defense responses most affected by NO reduction during the incompatible interaction were decreased H 2 O 2 levels during the oxidative burst and a blockage of Phe ammonia lyase expression, the key enzyme in the general phenylpropanoid pathway. Expression of the NOD furthermore blocked UV light-induced Phe ammonia lyase and chalcone synthase gene expression, indicating a general signaling function of NO in the activation of the phenylpropanoid pathway. NO possibly functions in incompatible plant-pathogen interactions by inhibiting the plant antioxidative machinery, and thereby ensuring locally prolonged H 2 O 2 levels. Additionally, albeit to a lesser extent, we observed decreases in salicylic acid production, a diminished development of hypersensitive cell death, and a delay in pathogenesis-related protein 1 expression during these NO-deficient plant-pathogen interactions. Therefore, this genetic approach confirms that NO is an important regulatory component in the signaling network of plant defense responses.Plants have evolved several mechanisms to defend themselves from bacterial or fungal invasion. The rapid recognition of pathogenic microbes is based on the interaction of products from a pathogen-derived avirulence gene and a plant-derived resistance gene and represents a prerequisite to specific resistance in incompatible plant-pathogen interactions (Flor, 1956). The multicomponent defense responses associated with specific resistance include a burst of reactive oxygen intermediates (ROI; Lamb and Dixon, 1997), transcriptional activation of defense genes encoding phenylpropanoid pathway enzymes, lytic and antimicrobial pathogenesis-related (PR) proteins (Lamb et al., 1989), increase of intracellular levels of salicylic acid (SA; Malamy et al., 1990; Métraux et al., 1990), and development of the hypersensitive response (HR). The HR results in the rapid appearance of a dry, necrotic lesion at the infection site that is clearly delimited from surrounding healthy tissue and is thought to contribute to the limitation of pathogen spread (Keen, 1990).One of the earliest events following pathogen recognition is a burst of oxidative metabolism leading to the generation of su...

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Section: Growth Of Plant-pathogens and Infectionmentioning

confidence: 99%

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confidence: 99%

Genetic Elucidation of Nitric Oxide Signaling in Incompatible Plant-Pathogen Interactions

et al. 2004

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“…Examples include the FHP protein t Present address: Krebs Institute for Biomolecular Research, Department of Alcaligenes eutrophus (Probst et al, 1979;Cramm et al, 1994;Ermler et al, 1995), HmpX of Erwinia chrysanthemi (Favey et al, 1995), Hmp of Bacillus subtilis (LaCelle et al, 1996), and the haemoglobins of the yeasts Candida sp. (Oshino et al, 1973a, b;Iwaasa et al, 1992) and Saccharomyces cerevisiae (Zhu & Riggs, 1992).…”

Section: Introductionmentioning

confidence: 99%

Escherichia coli flavohaemoglobin (Hmp) reduces cytochrome c and Fe(III)-hydroxamate K by electron transfer from NADH via FAD: sensitivity of oxidoreductase activity to haem-bound dioxygen

et al. 1997

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JapanEscherichia coli flavohaemoglobin (Hmp) reduced purified mitochondria1 cytochrome c aerobically in a reaction that was not substantially inhibited by superoxide dismutase, demonstrating that superoxide anion, the product of 0, reduction by Hmp, did not contribute markedly to cytochrome c reduction. Cytochrome c was reduced by Hmp even in the presence of 0 5 mM CO, when the haem B was locked in the ferrous, low-spin state, demonstrating that electron transfer to cytochrome c from NADH was via FAD, not haem. Hmp also reduced the ferrisiderophore complex Fe(lll)-hydroxamate K from Rhizobium leguminosanrm bv. wiciae anaerobically in a CO-insensitive manner, but at low rates and with low affinity for this substrate. The NADH+ytochrome c oxidoreductase activity of Hmp was slightly sensitive to the binding and reduction of 0, at the haem. The V-of cytochrome c reduction fell from 7.1 s-l in the presence of 0 5 mM CO to 5 0 s'l in the presence of 100 pM O,, with no significant change in Km for cytochrome c (68 to 7.3 pM, respectively). 0, at near-micromolar concentrations diminished cytochrome c reduction to a similar extent as did 100 pM 0 , . Thus, Hmp acts as a reductase of broad specificity, apparently without involvement of electron transfer via the globinlike haem. These data are consistent with the hypothesis that Hmp could act as an intracellular sensor of 0, since, in the absence of O, , electron flux from FAD to other electron acceptors increases. However, the nature of such acceptors in wivo is not known and alternative models for 0, sensing are also considered.

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“…In 1986, Wakabayashi and coauthors reported the presence of a bacterial hemoglobin (Vgb) in Vitreoscilla cells, challenging the view that the distribution of hemoglobin was restricted to eukaryotes (for a review, see reference 37). Other hemoglobins found in many bacteria are two-domain proteins (6,11,27,44). The N terminus contains the heme domain, whereas the C terminus contains a reductase domain with potential binding sites for flavin (flavin adenine dinucleotide) and NAD(P)H (9).…”

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confidence: 99%

Paraquat regulation of hmp (flavohemoglobin) gene expression in Escherichia coli K-12 is SoxRS independent but modulated by sigma S

et al. 1997

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We report the first example of a gene, hmp, encoding a soluble flavohemoglobin in Escherichia coli K-12, which is up-regulated by paraquat in a SoxRS-independent manner. Unlike what is found for other paraquatinducible genes, high concentrations of paraquat (200 M) were required to increase the level of hmp expression, and maximal induction was observed only after 20 min of exposure to paraquat. Neither a mutation in soxS nor one in soxR prevented the paraquat-dependent increase in ⌽(hmp-lacZ) expression, but either mutant allele delayed full expression of ⌽(hmp-lacZ) activity after paraquat addition. Induction of hmp by paraquat was demonstrated in aerobically grown cultures during exponential growth and the stationary phase, thus revealing two Sox-independent regulatory mechanisms. Induction of hmp by paraquat in the stationary phase was dependent on the global regulator of stationary-phase gene expression, RpoS ( s ). However, a mutation in rpoS did not prevent an increase in hmp expression by paraquat in exponentially growing cells. Induction of s in the exponential phase by heat shock also induced ⌽(hmp-lacZ) expression in the presence of paraquat, supporting the role of s in one of the regulatory mechanisms. Mutations in oxyR or rob, known regulators of several stress promoters in E. coli, had no effect on the induction of hmp by paraquat. Other known superoxide-generating agents (plumbagin, menadione, and phenazine methosulfate) were not effective in inducing hmp expression.

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Flavohaemoglobin HmpX: a new pathogenicity determinant in Erwinia chrysanthemi strain 3937

Cited by 70 publications

References 35 publications

Genetic Elucidation of Nitric Oxide Signaling in Incompatible Plant-Pathogen Interactions

Genetic Elucidation of Nitric Oxide Signaling in Incompatible Plant-Pathogen Interactions

Escherichia coli flavohaemoglobin (Hmp) reduces cytochrome c and Fe(III)-hydroxamate K by electron transfer from NADH via FAD: sensitivity of oxidoreductase activity to haem-bound dioxygen

Paraquat regulation of hmp (flavohemoglobin) gene expression in Escherichia coli K-12 is SoxRS independent but modulated by sigma S

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