High affinity binding of a fungal oligopeptide elicitor to parsley plasma membranes triggers multiple defense responses

Nürnberger, Thorsten; Nennstiel, Dirk; Jabs, Thorsten; Sacks, Wendy R.; Hahlbrock, Klaus; Scheel, Dierk

doi:10.1016/0092-8674(94)90423-5

Cited by 553 publications

(419 citation statements)

References 41 publications

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“…A comparably high degree of correlation between elicitor and displacement activities of ligand derivatives was found for other elicitors and their binding sites as well (Cheong and Hahn, 1991;Nürnberger et al, 1994;Bourque et al, 1998;Kooman-Gersmann et al, 1998;Meindl et al, 2000). Unfortunately, the preparation of tobacco protoplasts caused PR gene expression in the absence of harpin Psph (data not shown); hence, it was impossible to determine if protoplasts would respond to harpin Psph treatment in a manner similar to intact cells.…”

Section: A Harpin Binding Site Involved In Pr Gene Expression In Tobaccomentioning

confidence: 98%

“…The precipitated protein was resuspended in 5 mM Mes buffer, pH 5.5, and desalted using PD-10 columns (Amersham Pharmacia, Freiburg, Germany). This procedure allowed purification to more than 95% homogeneity according to SDS-PAGE/ silver staining and reverse phase HPLC analysis (Nürnberger et al, 1994).…”

Section: Elicitor Preparationmentioning

confidence: 99%

“…Solid phase peptide synthesis with N-␣-9-fluorophenylmethoxycarbonyl (Fmoc)-protected amino acids was performed with an Economy Peptide Synthesizer EPS 221 (ABIMED, Langen, Germany) according to the manufacturer's instructions. Synthesized peptides were purified to homogeneity as described (Nürnberger et al, 1994).…”

Section: Elicitor Preparationmentioning

confidence: 99%

“…Labeling with Na 125 I to a specific radioactivity of 2200 Ci/mmol was performed by Biotrend Chemikalien (Köln, Germany). Tobacco BY2 cells (6 days old) were used for the preparation of microsomes as described (Nürnberger et al, 1994). The microsomal pellet recovered from 150 g of frozen tobacco cells was resuspended in 5 mL of 20 mM sodium phosphate and 100 mM NaCl, pH 7.0.…”

Section: Iodination Of Harpin Psph Microsomal Membrane Preparationmentioning

confidence: 99%

“…If not indicated otherwise, binding was initiated by the addition of 100 nM 125 I-harpin Psph . The binding reaction was terminated by adding 5 mL of ice-cold buffer, and membranes were harvested by filtration on Whatman GF/B glass filters (Maidstone, UK) preblocked with 5% BSA in binding buffer (Nürnberger et al, 1994). Subsequently, filters were subjected to ␥-counting in a Wizard counter (Amersham Pharmacia).…”

Section: Iodination Of Harpin Psph Microsomal Membrane Preparationmentioning

confidence: 99%

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A Harpin Binding Site in Tobacco Plasma Membranes Mediates Activation of the Pathogenesis-Related Gene HIN1 Independent of Extracellular Calcium but Dependent on Mitogen-Activated Protein Kinase Activity

Lee¹,

Klessig²,

Nürnberger³

2001

The Plant Cell

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Harpin from the bean halo-blight pathogen Pseudomonas syringae pv phaseolicola (harpin Psph ) elicits the hypersensitive response and the accumulation of pathogenesis-related gene transcripts in the nonhost plant tobacco. Here, we report the characterization of a nonproteinaceous binding site for harpin Psph in tobacco plasma membranes, which is assumed to mediate the activation of plant defense responses in a receptor-like manner. Binding of 125 I-harpin Psph to tobacco microsomal membranes (dissociation constant ‫؍‬ 425 nM) and protoplasts (dissociation constant ‫؍‬ 380 nM) was specific, reversible, and saturable. A close correlation was found between the abilities of harpin Psph fragments to elicit the transcript accumulation of the pathogenesis-related tobacco gene HIN1 and to compete for binding of 125 Iharpin Psph to its binding site. Another elicitor of the hypersensitive response and HIN1 induction in tobacco, the Phytophthora megasperma -derived ␤ -elicitin ␤ -megaspermin, failed to bind to the putative harpin Psph receptor. In contrast to activation by ␤ -megaspermin, harpin Psph -induced activation of the 48-kD salicylic acid-responsive mitogen-activated protein kinase (MAPK) and HIN1 transcript accumulation were independent of extracellular calcium. Moreover, use of the MAPK kinase inhibitor U0126 revealed that MAPK activity was essential for pathogenesis-related gene expression in harpin Psph -treated tobacco cells. Thus, a receptor-mediated MAPK-dependent signaling pathway may mediate the activation of plant defense responses induced by harpin Psph .

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Section: A Harpin Binding Site Involved In Pr Gene Expression In Tobaccomentioning

confidence: 98%

Section: Elicitor Preparationmentioning

confidence: 99%

Section: Elicitor Preparationmentioning

confidence: 99%

Section: Iodination Of Harpin Psph Microsomal Membrane Preparationmentioning

confidence: 99%

Section: Iodination Of Harpin Psph Microsomal Membrane Preparationmentioning

confidence: 99%

See 3 more Smart Citations

A Harpin Binding Site in Tobacco Plasma Membranes Mediates Activation of the Pathogenesis-Related Gene HIN1 Independent of Extracellular Calcium but Dependent on Mitogen-Activated Protein Kinase Activity

Lee¹,

Klessig²,

Nürnberger³

2001

The Plant Cell

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Pathogen-induced programmed cell death in plants, a possible defense mechanism

et al. 1997

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As much as the definition of life may be controversial, the definition of death also may prove problematic. In recent years it became apparent that the death of a living cell may follow more than one possible scenario: it may result from an externally applied physical injury (an accidental death), or it may be the outcome of activating an internal pathway for cell suicide (a programmed death). That cells can participate in their own execution may indicate that certain types of cell deaths that were previously considered to be caused by foreign agents such as pathogens or drugs may actually result from the activation of a programmed cell death pathway that is normally latent in cells. Here, we describe the activation of such a cell suicide pathway in plant cells upon the recognition of an invading pathogen. We discuss the possible use of this pathway as a defense mechanism against infection and the possibility that in many ways the use of this type of cell death in plants is functionally analogous to that used by mammalian cells in response to infection by pathogens. Dev. Genet. 21:279–289, 1997. © 1997 Wiley‐Liss, Inc.

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Oligoglucoside elicitor-mediated activation of plant defense

Ebel

1998

Bioessays

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High affinity binding of a fungal oligopeptide elicitor to parsley plasma membranes triggers multiple defense responses

Cited by 553 publications

References 41 publications

A Harpin Binding Site in Tobacco Plasma Membranes Mediates Activation of the Pathogenesis-Related Gene HIN1 Independent of Extracellular Calcium but Dependent on Mitogen-Activated Protein Kinase Activity

A Harpin Binding Site in Tobacco Plasma Membranes Mediates Activation of the Pathogenesis-Related Gene HIN1 Independent of Extracellular Calcium but Dependent on Mitogen-Activated Protein Kinase Activity

Pathogen-induced programmed cell death in plants, a possible defense mechanism

Oligoglucoside elicitor-mediated activation of plant defense

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