scholarly journals Riboflavin Induces Disease Resistance in Plants by Activating a Novel Signal Transduction Pathway

2000 ◽  
Vol 90 (8) ◽  
pp. 801-811 ◽  
Author(s):  
H. Dong ◽  
S. V. Beer
Keyword(s):  
Signal Transduction ◽  
Protein Kinase ◽  
Induced Resistance ◽  
Pseudomonas Syringae ◽  
Kinase Inhibitor ◽  
Signal Transduction Pathway ◽  
Systemic Resistance ◽  
Transduction Pathway ◽  
Pr Genes ◽  
Npr1 Gene

The role of riboflavin as an elicitor of systemic resistance and an activator of a novel signaling process in plants was demonstrated. Following treatment with riboflavin, Arabidopsis thaliana developed systemic resistance to Peronospora parasitica and Pseudomonas syringae pv. Tomato, and tobacco developed systemic resistance to Tobacco mosaic virus (TMV) and Alternaria alternata. Riboflavin, at concentrations necessary for resistance induction, did not cause cell death in plants or directly affect growth of the culturable pathogens. Riboflavin induced expression of pathogenesis-related (PR) genes in the plants, suggesting its ability to trigger a signal transduction pathway that leads to systemic resistance. Both the protein kinase inhibitor K252a and mutation in the NIM1/NPR1 gene which controls transcription of defense genes, impaired responsiveness to riboflavin. In contrast, riboflavin induced resistance and PR gene expression in NahG plants, which fail to accumulate salicylic acid (SA). Thus, riboflavin-induced resistance requires protein kinase signaling mechanisms and a functional NIM1/NPR1 gene, but not accumulation of SA. Riboflavin is an elicitor of systemic resistance, and it triggers resistance signal transduction in a distinct manner.

scholarly journals Lactosylceramide-enriched glycosphingolipid signaling domain mediates superoxide generation from human neutrophils

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1454-1464 ◽  
Author(s):  
Kazuhisa Iwabuchi ◽  
Isao Nagaoka
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase Inhibitor ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Superoxide Generation ◽  
Kinase C ◽  
Signaling Domain

This study is focused on the functional significance of neutrophil lactosylceramide (LacCer)–enriched microdomains, which are involved in the initiation of a signal transduction pathway leading to superoxide generation. Treatment of neutrophils with anti-LacCer antibody, T5A7 or Huly-m13, induced superoxide generation from the cells, which was blocked by PP1, a Src kinase inhibitor; wortmannin, a phosphatidylinositol-3 kinase inhibitor; SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor; and H7, an inhibitor for protein kinase C. When promyelocytic leukemia HL-60 cells were differentiated into neutrophilic lineage by dimethyl sulfoxide (DMSO) treatment, they acquired superoxide-generating activity but did not respond to anti-LacCer antibodies. Density gradient centrifugation revealed that LacCer and Lyn were recovered in detergent-insoluble membrane (DIM) of neutrophils and DMSO-treated HL-60 cells. However, immunoprecipitation experiments indicated that LacCer was associated with Lyn in neutrophils but not in DMSO-treated HL-60 cells. Interestingly, T5A7 induced the phosphorylation of Lyn in neutrophils but not in DMSO-treated HL-60 cells. Moreover, T5A7 induced the phosphorylation of p38 MAPK in neutrophils. T5A7-induced Lyn phosphorylation in neutrophil DIM fraction was significantly enhanced by cholesterol depletion or sequestration with methyl-β-cyclodextrin or nystatin. Collectively, these data suggest that neutrophils are characterized by the presence of cell surface LacCer-enriched glycosphingolipid signaling domain coupled with Lyn and that the ligand binding to LacCer induces the activation of Lyn, which may be suppressibly regulated by cholesterol, leading to superoxide generation through the phosphatidylinositol-3 kinase–, p38 MAPK–, and protein kinase C–dependent signal transduction pathway.

Far1 and Fus3 link the mating pheromone signal transduction pathway to three G1-phase Cdc28 kinase complexes

1993 ◽  
Vol 13 (9) ◽  
pp. 5659-5669 ◽  
Author(s):  
M Tyers ◽  
B Futcher
Keyword(s):  
Signal Transduction ◽  
Protein Kinase ◽  
Signal Transduction Pathway ◽  
Mitogen Activated Protein Kinase ◽  
G1 Phase ◽  
Transduction Pathway ◽  
Yeast Saccharomyces Cerevisiae ◽  
Alpha Factor ◽  
Mitogen Activated Protein

In the yeast Saccharomyces cerevisiae, the Cdc28 protein kinase controls commitment to cell division at Start, but no biologically relevant G1-phase substrates have been identified. We have studied the kinase complexes formed between Cdc28 and each of the G1 cyclins Cln1, Cln2, and Cln3. Each complex has a specific array of coprecipitated in vitro substrates. We identify one of these as Far1, a protein required for pheromone-induced arrest at Start. Treatment with alpha-factor induces a preferential association and/or phosphorylation of Far1 by the Cln1, Cln2, and Cln3 kinase complexes. This induced interaction depends upon the Fus3 protein kinase, a mitogen-activated protein kinase homolog that functions near the bottom of the alpha-factor signal transduction pathway. Thus, we trace a path through which a mitogen-activated protein kinase regulates a Cdc2 kinase.

scholarly journals Induced Systemic Resistance in Arabidopsis thaliana Against Pseudomonas syringae pv. tomato by 2,4-Diacetylphloroglucinol-Producing Pseudomonas fluorescens

2012 ◽  
Vol 102 (4) ◽  
pp. 403-412 ◽  
Author(s):  
David M. Weller ◽  
Dmitri V. Mavrodi ◽  
Johan A. van Pelt ◽  
Corné M. J. Pieterse ◽  
Leendert C. van Loon ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Pseudomonas Fluorescens ◽  
Induced Resistance ◽  
Pseudomonas Syringae ◽  
Induced Systemic Resistance ◽  
Signal Transduction Pathway ◽  
Systemic Resistance ◽  
Wild Type ◽  
Challenge Inoculation ◽  
Dependent Signal

Pseudomonas fluorescens strains that produce the polyketide antibiotic 2,4-diacetylphloroglucinol (2,4-DAPG) are among the most effective rhizobacteria that suppress root and crown rots, wilts, and damping-off diseases of a variety of crops, and they play a key role in the natural suppressiveness of some soils to certain soilborne pathogens. Root colonization by 2,4-DAPG-producing P. fluorescens strains Pf-5 (genotype A), Q2-87 (genotype B), Q8r1-96 (genotype D), and HT5-1 (genotype N) produced induced systemic resistance (ISR) in Arabidopsis thaliana accession Col-0 against bacterial speck caused by P. syringae pv. tomato. The ISR-eliciting activity of the four bacterial genotypes was similar, and all genotypes were equivalent in activity to the well-characterized strain P. fluorescens WCS417r. The 2,4-DAPG biosynthetic locus consists of the genes phlHGF and phlACBDE. phlD or phlBC mutants of Q2-87 (2,4-DAPG minus) were significantly reduced in ISR activity, and genetic complementation of the mutants restored ISR activity back to wild-type levels. A phlF regulatory mutant (overproducer of 2,4-DAPG) had ISR activity equivalent to the wild-type Q2-87. Introduction of DAPG into soil at concentrations of 10 to 250 μM 4 days before challenge inoculation induced resistance equivalent to or better than the bacteria. Strain Q2-87 induced resistance on transgenic NahG plants but not on npr1-1, jar1, and etr1 Arabidopsis mutants. These results indicate that the antibiotic 2,4-DAPG is a major determinant of ISR in 2,4-DAPG-producing P. fluorescens, that the genotype of the strain does not affect its ISR activity, and that the activity induced by these bacteria operates through the ethylene- and jasmonic acid-dependent signal transduction pathway.

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