Tomato Mutants Altered in Bacterial Disease Resistance Provide Evidence for a New Locus Controlling Pathogen Recognition

Salmeron, John M.; Barker, Susan J.; Carland, Francine M.; Mehta, Anand Y.; Staskawicz, Brian J.

doi:10.2307/3869931

Cited by 44 publications

(63 citation statements)

References 13 publications

(34 reference statements)

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“…One of these PTO homologs, FEN, confers sensitivity to the organophosphorous insecticide fenthion. The evidence that FEN is a separate gene comes from mutational analyses (35) and from the demonstration that a cDNA clone with -80% homology to PTO confers sensitivity to the insecticide (36 avrRpt2, was identified by isolation of Ara-r bidopsis mutants that did not exhibit HR in1 response to P. syringae strains carrying avr-' Rpt2. The RPS2 gene was then cloned by means of a map-based strategy similar in concept to the method used to identify the tomato PTO gene (31).…”

Section: Cloning and Characterizationmentioning

confidence: 99%

Molecular Genetics of Plant Disease Resistance

Staskawicz

Ausubel

Baker

et al. 1995

Science

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842

444

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Plant breeders have used disease resistance genes ( R genes) to control plant disease since the turn of the century. Molecular cloning of R genes that enable plants to resist a diverse range of pathogens has revealed that the proteins encoded by these genes have several features in common. These findings suggest that plants may have evolved common signal transduction mechanisms for the expression of resistance to a wide range of unrelated pathogens. Characterization of the molecular signals involved in pathogen recognition and of the molecular events that specify the expression of resistance may lead to novel strategies for plant disease control.

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Section: Cloning and Characterizationmentioning

confidence: 99%

Molecular Genetics of Plant Disease Resistance

Staskawicz

Ausubel

Baker

et al. 1995

Science

Self Cite

842

444

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“…6A, compare third and last column of each time point). These assays were also carried out in protoplasts from prf-3 tomato plants which have a mutation in the Prf gene (54,55). This gene is required for Pto-mediated cell death in response to AvrPto, and cell death is not induced in prf-3 plants when treated with AvrPto (10,54,55).…”

Section: Deletion Of the T-loop Extension Causes Localization Of Adi3mentioning

confidence: 99%

The T-loop Extension of the Tomato Protein Kinase AvrPto-dependent Pto-interacting Protein 3 (Adi3) Directs Nuclear Localization for Suppression of Plant Cell Death

Ek-Ramos

Ávila-Pacheco

Cheng

et al. 2010

Journal of Biological Chemistry

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In tomato (Solanum lycopersicum), resistance to Pseudomonas syringae pv. tomato is elicited by the interaction of the host Pto kinase with the pathogen effector protein AvrPto, which leads to various immune responses including localized cell death termed the hypersensitive response. The AGC kinase Adi3 functions to suppress host cell death and interacts with Pto only in the presence of AvrPto. The cell death suppression (CDS) activity of Adi3 requires phosphorylation by 3-phosphoinositide-dependent protein kinase 1 (Pdk1) and loss of Adi3 function is associated with the hypersensitive response cell death initiated by the Pto/AvrPto interaction. Here we studied the relationship between Adi3 cellular localization and its CDS activity. Adi3 is a nuclear-localized protein, and this localization is dictated by a nuclear localization signal found in the Adi3 T-loop extension, an ϳ80 amino acid insertion into the T-loop, or activation loop, which is phosphorylated for kinase activation. Nuclear localization of Adi3 is required for its CDS activity and loss of nuclear localization causes elimination of Adi3 CDS activity and induction of cell death. This nuclear localization of Adi3 is dependent on Ser-539 phosphorylation by Pdk1 and nonnuclear Adi3 is found in punctate structures throughout the cell. Our data support a model in which Pdk1 phosphorylation of Adi3 directs nuclear localization for CDS and that disruption of Adi3 nuclear localization may be a mechanism for induction of cell death such as that during the Pto/AvrPto interaction.During the resistance response of plants to pathogens, programmed cell death (PCD) 2 occurs as part of the hypersensitive response (HR), which functions to limit pathogen spread (1, 2). It has been over 100 years since the first description of the HR and its associated cell death (3). However, not until relatively recent times has the search for genes and pathways regulating PCD during the HR received much attention. This search has been difficult, but has identified several kinases and transcription factors involved in PCD (1, 4, 5) as well as lipid biosynthetic genes that produce lipid second messengers regulating PCD (6 -9). In tomato (Solanum lycopersicum), the causative agent of bacterial speck disease is Pseudomonas syringae pv. tomato (Pst). Interaction of the tomato resistance protein kinase Pto with the Pst effector protein AvrPto brings about the HR and resistance to Pst (10). Studies have been undertaken to identify genes involved in PCD associated with Pto-mediated HR and revealed a downstream MAP kinase, MAPKKK␣, that functions in the induction of cell death during both resistance and susceptibility (11).Another gene that was identified as a Pto-interacting protein was the tomato protein kinase Adi3, which only interacts with Pto in the presence of AvrPto (12). Subsequently, we have shown Adi3 to function as a negative regulator of plant cell death (13) and thus, it may be the functional homologue of PKB (aka Akt), a major PCD suppressor in mammals (13-15). Adi3 is phospho...

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“…tomato (avrPto) interaction, is based on a gene-for-gene relationship (27 (21). A potential myristoylation site (20,22) (30). Presumably, this tandem repetition of related genes has evolved by gene duplication events followed by sequence divergence (31).…”

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confidence: 99%