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Phospholipidase D? Negatively Regulates the Function of Resistance to Pseudomonas syringae pv. Maculicola 1 (RPM1).

ABSTRACT: RPM1 is a plant immune receptor that specially recognizes pathogen-released effectors to activate effector-triggered immunity (ETI) in Arabidopsis thaliana. RPM1 triggers ETI and hypersensitive response (HR) for disease resistance. Previous reports indicated that Phospholipase D (PLD) positively regulated RPM1-mediated HR. However, single, double, and triple pld knock-out mutants of 12 members of the PLD family in A. thaliana did not show suppressed RPM1-mediated HR, indicating the functional redundancy among PLD members. In this study, we revealed that PLD could negatively regulate the function of RPM1. We found that RPM1 interacted with PLD?, but did not interact with PLD?1, PLD?2, and PLD?3. Overexpression of PLD? conducted to a reduction of protein level and corresponding activity of RPM1. We found that abscisic acid (ABA) reduced the protein level of RPM1, and the ABA-induced RPM1 reduction required PLD activity and PLD-derived phosphatidic acid (PA). Our study shows that PLD plays both negative and positive roles regulating the protein level and activity of RPM1 during stress responses in plants. PLD proteins are regulating points to integrate the abiotic and biotic responses of plants.

SUBMITTER: Yuan X

PROVIDER: S-EPMC6345720 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Plant intracellular innate immune receptor Resistance to Pseudomonas syringae pv. maculicola 1 (RPM1) is activated at, and functions on, the plasma membrane.

Project description:Plants deploy intracellular innate immune receptors to recognize pathogens and initiate disease resistance. These nucleotide-binding, leucine-rich repeat (NB-LRR) proteins are activated by pathogen effector proteins that are delivered into the host cell to suppress host defense responses. Little is known about the sites and mechanisms of NB-LRR activation, but some NB-LRR proteins can function inside the plant nucleus. We demonstrate that RPM1 is activated on the plasma membrane and does not relocalize to the nucleus. An autoactive RPM1(D505V) allele that recapitulates key features of normal RPM1 activation also resides on the plasma membrane. There is no detectable relocalization of activated RPM1 to the nucleus. Hindering potential nuclear entry of RPM1-Myc did not affect either its effector-triggered hypersensitive-response (HR) cell death or its disease resistance functions, further suggesting that nuclear translocation is not required for RPM1 function. RPM1 tethered onto the plasma membrane with a dual acylated N-terminal epitope tag retained the ability to mediate HR, consistent with this RPM1 function being activated on the plasma membrane. Plant NB-LRR proteins can thus function at various locations in the cell.

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Housekeeping gene sequencing and multilocus variable-number tandem-repeat analysis to identify subpopulations within Pseudomonas syringae pv. maculicola and Pseudomonas syringae pv. tomato that correlate with host specificity.

Project description:Pseudomonas syringae pv. maculicola causes bacterial spot on Brassicaceae worldwide, and for the last 10 years severe outbreaks have been reported in the Loire Valley, France. P. syringae pv. maculicola resembles P. syringae pv. tomato in that it is also pathogenic for tomato and causes the same types of symptoms. We used a collection of 106 strains of P. syringae to characterize the relationships between P. syringae pv. maculicola and related pathovars, paying special attention to P. syringae pv. tomato. Phylogenetic analysis of gyrB and rpoD gene sequences showed that P. syringae pv. maculicola, which causes diseases in Brassicaceae, forms six genetic lineages within genomospecies 3 of P. syringae strains as defined by L. Gardan et al. (Int. J. Syst. Bacteriol. 49[Pt 2]:469-478, 1999), whereas P. syringae pv. tomato forms two distinct genetic lineages. A multilocus variable-number tandem-repeat (VNTR) analysis (MLVA) conducted with eight minisatellite loci confirmed the genetic structure obtained with rpoD and gyrB sequence analyses. These results provide promising tools for fine-scale epidemiological studies on diseases caused by P. syringae pv. maculicola and P. syringae pv. tomato. The two pathovars had distinct host ranges; only P. syringae pv. maculicola strains were pathogenic for Brassicaceae. A subpopulation of P. syringae pv. maculicola strains that are pathogenic for Pto-expressing tomato plants were shown to lack avrPto1 and avrPtoB or to contain a disrupted avrPtoB homolog. Taking phylogenetic and pathological features into account, our data suggest that the DC3000 strain belongs to P. syringae pv. maculicola. This study shows that P. syringae pv. maculicola and P. syringae pv. tomato appear multiclonal, as they did not diverge from a single common ancestral group within the ancestral P. syringae genomospecies 3, and suggests that pathovar specificity within P. syringae may be due to independent genetic events.

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The Genetic Network Controlling the Arabidopsis Transcriptional Response to Pseudomonas syringae pv. maculicola

Project description:Expression profiling of wild-type plants and mutants with defects in key components of the defense signaling network was used to model the Arabidopsis network 24 hours after infection by Pseudomonas syringae pv. maculicola strain Psm ES4326. Results using the Affymetrix ATH1 array revealed that expression levels of most pathogen-responsive genes were affected by mutations in coi1, ein2, npr1, pad4, or sid2. These five mutations defined a small number of different expression patterns displayed by the majority of pathogen-responsive genes. P. syringae pv. tomato strain Pst DC3000 elicited a much weaker salicylic acid response than Psm ES4326. Additional mutants were profiled using a custom array. Profiles of pbs3 and ndr1 revealed major effects of these mutations and allowed PBS3 and NDR1 to be placed between the EDS1/PAD4 node and the SA synthesis node in the defense network. Comparison of coi1, dde2, and jar1 profiles showed that many genes were affected by coi1, but very few were affected by dde2 or jar1. Profiles of coi1 plants infected with Psm ES4326 were very similar to those of wild-type plants infected with bacteria unable to produce the phytotoxin coronatine, indicating that essentially all COI1-dependent gene expression changes in this system are caused by coronatine.

2008-07-18 | GSE11009 | GEO

Nucleotide sequence and evolution of the five-plasmid complement of the phytopathogen Pseudomonas syringae pv. maculicola ES4326.

Project description:Plasmids are transmissible, extrachromosomal genetic elements that are often responsible for environmental or host-specific adaptations. In order to identify the forces driving the evolution of these important molecules, we determined the complete nucleotide sequence of the five-plasmid complement of the radish and Arabidopsis pathogen Pseudomonas syringae pv. maculicola ES4326 and conducted an intraspecific comparative genomic analysis. To date, this is the most complex fully sequenced plasmid complement of any gram-negative bacterium. The plasmid complement comprises two pPT23A-like replicons, pPMA4326A (46,697 bp) and pPMA4326B (40,110 bp); a pPS10-like replicon, pPMA4326C (8,244 bp); and two atypical, replicase-deficient replicons, pPMA4326D (4,833 bp) and pPMA4326E (4,217 bp). A complete type IV secretion system is found on pPMA4326A, while the type III secreted effector hopPmaA is present on pPMA4326B. The region around hopPmaA includes a shorter hopPmaA homolog, insertion sequence (IS) elements, and a three-element cassette composed of a resolvase, an integrase, and an exeA gene that is also present in several human pathogens. We have also identified a novel genetic element (E622) that is present on all but the smallest plasmid (pPMA4326E) that has features of an IS element but lacks an identifiable transposase. This element is associated with virulence-related genes found in a wide range of P. syringae strains. Comparative genomic analyses of these and other P. syringae plasmids suggest a role for recombination and integrative elements in driving plasmid evolution.

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Project description:Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae. AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhanced pathogen-induced MAPK activities, increased callose deposition in response to pathogen-associated molecular patterns or to P. syringae pv. tomato (Pto) DC3000, and enhanced resistance to bacterial infection with Pto. We also reveal the impact of AP2C1 on the global transcriptional reprogramming of transcription factors during Pto infection. Importantly, ap2c1 plants show salicylic acid-independent transcriptional reprogramming of several defense genes and enhanced ethylene production in response to Pto. This study pinpoints the specificity of MAPK regulation by the different MAPK phosphatases AP2C1 and MKP1, which control the same MAPK substrates, nevertheless leading to different downstream events. We suggest that precise and specific control of defined MAPKs by MAPK phosphatases during plant challenge with pathogenic bacteria can strongly influence plant resistance.

| S-EPMC5444444 | biostudies-literature

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