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Oxylipins produced by the 9-lipoxygenase pathway in Arabidopsis regulate lateral root development and defense responses through a specific signaling cascade
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In this study the Arabidopsis 9-Lipoxygenase pathway was found to regulate lateral root development and defense responses through a specific signaling pathway. A mutant, noxy2, that was defective in responding to 9-hydroxilinolenic acid (in a root-waving assay) was found not only to display alterations in root development, but also enhanced susceptibility to Pseudomonas.
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Vellosillo T., Martinez M., Lopez M.A., Vicente J., Cascon T., Dolan L., Hamberg M., and Castresana C. Oxylipins produced by the 9-lipoxygenase pathway in Arabidopsis regulate lateral root development and defense responses through a specific signaling cascade. Plant Cell 19 (2007) 831-846. In this study the Arabidopsis 9-Lipoxygenase pathway was found to regulate lateral root development and defense responses through a specific signaling pathway. A mutant, noxy2, that was defective in responding to 9-hydroxilinolenic acid (in a root-waving assay) was found not only to display alterations in root development, but also enhanced susceptibility to Pseudomonas.
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Gao X., Starr J., Gobel C., Engelberth J., Feussner I., Tumlinson J., and Kolomiets M. Maize 9-lipoxygenase ZmLOX3 controls development, root-specific expression of defense genes, and resistance to root-knot nematodes. Mol Plant Microbe Interact 21 (2008) 98-109
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The authors review studies showing the production of oxylipins by microbial pathogens and their function as hormone-like signals to modulate development and infection.
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This paper illustrates that ABA enhances resistance by inducing stomatal closure to reduce pathogen entry, whereas coronatine interfere in this plant immune response helping to reopen plant stomatal to facilitate bacterial invasion.
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Melotto, M.1
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The BRI1-associated kinase 1, BAK1, has a brassinolide-independent role in plant cell-death control
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Authors report that the Arabidopsis thaliana brassinosteroid insensitive 1 (BRI1)-associated receptor kinase 1 (BAK1), which operates as a coreceptor of BRI1 in BL-dependent plant development, also regulates the containment of microbial infection-induced cell death. The role of BAK1 in plant cell death control is distinct from its BL-dependent role in plant development.
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Kemmerling B., Schwedt A., Rodriguez P., Mazzotta S., Frank M., Qamar S.A., Mengiste T., Betsuyaku S., Parker J.E., Mussig C., et al. The BRI1-associated kinase 1, BAK1, has a brassinolide-independent role in plant cell-death control. Curr Biol 17 (2007) 1116-1122. Authors report that the Arabidopsis thaliana brassinosteroid insensitive 1 (BRI1)-associated receptor kinase 1 (BAK1), which operates as a coreceptor of BRI1 in BL-dependent plant development, also regulates the containment of microbial infection-induced cell death. The role of BAK1 in plant cell death control is distinct from its BL-dependent role in plant development.
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Kemmerling, B.1
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The receptor-like kinase SERK3/BAK1 is a central regulator of innate immunity in plants
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In this study BAK1, is shown to be a component of plant MAMP-triggered immunity. BAK1 interacts with FLAGELLIN SENSING 2 (FLS2), the receptor of the bacterial MAMP flagellin, to trigger immunity. BAK1, is required for full responses to multiple MAMPs in Nicotiana benthamiana and for restriction of bacterial and oomycete infections.
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Heese A., Hann D.R., Gimenez-Ibanez S., Jones A.M., He K., Li J., Schroeder J.I., Peck S.C., and Rathjen J.P. The receptor-like kinase SERK3/BAK1 is a central regulator of innate immunity in plants. Proc Natl Acad Sci U S A 104 (2007) 12217-12222. In this study BAK1, is shown to be a component of plant MAMP-triggered immunity. BAK1 interacts with FLAGELLIN SENSING 2 (FLS2), the receptor of the bacterial MAMP flagellin, to trigger immunity. BAK1, is required for full responses to multiple MAMPs in Nicotiana benthamiana and for restriction of bacterial and oomycete infections.
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Proc Natl Acad Sci U S A
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A flagellin-induced complex of the receptor FLS2 and BAK1 initiates plant defence
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In this study, authors show that BAK1 interacts with the flagellin receptor FLS2 to activate flagellin-triggered responses. Plans carrying bak1 mutations show normal flagellin binding but reduced activation of MAMP-triggered immunity. BAK1 and FLS2 form a complex within the first minutes of stimulation with flagellin to initiate immunity.
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Chinchilla D., Zipfel C., Robatzek S., Kemmerling B., Nurnberger T., Jones J.D., Felix G., and Boller T. A flagellin-induced complex of the receptor FLS2 and BAK1 initiates plant defence. Nature 448 (2007) 497-500. In this study, authors show that BAK1 interacts with the flagellin receptor FLS2 to activate flagellin-triggered responses. Plans carrying bak1 mutations show normal flagellin binding but reduced activation of MAMP-triggered immunity. BAK1 and FLS2 form a complex within the first minutes of stimulation with flagellin to initiate immunity.
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Nature
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Chinchilla, D.1
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Pseudomonas syringae type III effector AvrRpt2 alters Arabidopsis thaliana auxin physiology
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This paper illustrates that the Pseudomonas syringae type III effector AvrRpt2 modulates host auxin physiology to promote disease. Constitutive expression of AvrRpt2 in Arabidopsis thaliana rps2 mutants (lacking a functional RPS2 gene), increases the level of free indole acetic acid and produces phenotypes reminiscent of altered auxin physiology. Elevated levels of auxins promote PstDC3000 virulence.
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Chen Z., Agnew J.L., Cohen J.D., He P., Shan L., Sheen J., and Kunkel B.N. Pseudomonas syringae type III effector AvrRpt2 alters Arabidopsis thaliana auxin physiology. Proc Natl Acad Sci U S A 104 (2007) 20131-20136. This paper illustrates that the Pseudomonas syringae type III effector AvrRpt2 modulates host auxin physiology to promote disease. Constitutive expression of AvrRpt2 in Arabidopsis thaliana rps2 mutants (lacking a functional RPS2 gene), increases the level of free indole acetic acid and produces phenotypes reminiscent of altered auxin physiology. Elevated levels of auxins promote PstDC3000 virulence.
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Proc Natl Acad Sci U S A
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Chen, Z.1
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