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Jasmonate and related signalling compounds have a crucial role in both host immunity and development in plants, but the molecular details of the signalling mechanism are poorly understood. Here we identify members of the jasmonate ZIM-domain (JAZ) protein family as key regulators of jasmonate signalling. JAZ1 protein acts to repress transcription of jasmonate-responsive genes. Jasmonate treatment causes JAZ1 degradation and this degradation is dependent on activities of the SCF(COI1) ubiquitin ligase and the 26S proteasome. Furthermore, the jasmonoyl-isoleucine (JA-Ile) conjugate, but not other jasmonate-derivatives such as jasmonate, 12-oxo-phytodienoic acid, or methyl-jasmonate, promotes physical interaction between COI1 and JAZ1 proteins in the absence of other plant proteins. Our results suggest a model in which jasmonate ligands promote the binding of the SCF(COI1) ubiquitin ligase to and subsequent degradation of the JAZ1 repressor protein, and implicate the SCF(COI1)-JAZ1 protein complex as a site of perception of the plant hormone JA-Ile.

Metric spaces are generalized by many scholars. Recently, Khatami and Mirzavaziri use a mapping called t-definer to popularize the triangle inequality and give a generalization of the notion of a metric, which is called a ★-metric. In this paper, we prove that every ★-metric space is metrizable. Also, we study the total boundedness and completeness of ★-metric spaces.

Salicylic acid (SA)-mediated host immunity plays a central role in combating microbial pathogens in plants. Inactivation of SA-mediated immunity, therefore, would be a critical step in the evolution of a successful plant pathogen. It is known that mutations in conserved effector loci (CEL) in the plant pathogens Pseudomonas syringae (the ΔCEL mutation), Erwinia amylovora (the dspA/E mutation), and Pantoea stewartii subsp. stewartii (the wtsE mutation) exert particularly strong negative effects on bacterial virulence in their host plants by unknown mechanisms. We found that the loss of virulence in ΔCEL and dspA/E mutants was linked to their inability to suppress cell wall-based defenses and to cause normal disease necrosis in Arabidopsis and apple host plants. The ΔCEL mutant activated SA-dependent callose deposition in wild-type Arabidopsis but failed to elicit high levels of callose-associated defense in Arabidopsis plants blocked in SA accumulation or synthesis. This mutant also multiplied more aggressively in SA-deficient plants than in wild-type plants. The hopPtoM and avrE genes in the CEL of P. syringae were found to encode suppressors of this SA-dependent basal defense. The widespread conservation of the HopPtoM and AvrE families of effectors in various bacteria suggests that suppression of SA-dependent basal immunity and promotion of host cell death are important virulence strategies for bacterial infection of plants.

The areas in China with climates suitable for the potential distribution of the pest species red turpentine beetle (RTB) Dendroctonus valens LeConte (Coleoptera: Scolytidae) were predicted by CLIMEX based on historical climate data and future climate data with warming estimated. The model used a historical climate data set (1971–2000) and a simulated climate data set (2010–2039) provided by the Tyndall Centre for Climate Change (TYN SC 2.0). Based on the historical climate data, a wide area was available in China with a suitable climate for the beetle in which every province might contain suitable habitats for this pest, particularly all of the southern provinces. The northern limit of the distribution of the beetle was predicted to reach Yakeshi and Elunchun in Inner Mongolia, and the western boundary would reach to Keerkezi in Xinjiang Province. Based on a global-warming scenario, the area with a potential climate suited to RTB in the next 30 years (2010–2039) may extend further to the northeast. The northern limit of the distribution could reach most parts of south Heilongjiang Province, whereas the western limit would remain unchanged. Combined with the tendency for RTB to spread, the variation in suitable habitats within the scenario of extreme climate warming and the multiple geographical elements of China led us to assume that, within the next 30 years, RTB would spread towards the northeast, northwest, and central regions of China and could be a potentially serious problem for the forests of China.

It is poorly understood why a particular plant species is resistant to the vast majority of potential pathogens that infect other plant species, a phenomenon referred to as \"nonhost\" resistance. Here, we show that Arabidopsis NHO1, encoding a glycerol kinase, is required for resistance to and induced by Pseudomonas syringae isolates from bean and tobacco. NHO1 is also required for resistance to the fungal pathogen Botrytis cinerea, indicating that NHO1 is not limited to bacterial resistance. Strikingly, P. s. pv. tomato DC3000, an isolate fully virulent on Arabidopsis, actively suppressed the NHO1 expression. This suppression is abolished in coi1 plants, indicating that DC3000 required an intact jasmonic acid signaling pathway in the plant to suppress NHO1 expression. Constitutive overexpression of NHO1 led to enhanced resistance to this otherwise virulent bacterium. The presence of avrB in DC3000, which activates a cultivar-specific \"gene-for-gene\" resistance in Arabidopsis, restored the induction of NHO1 expression. Thus, NHO1 is deployed for both general and specific resistance in Arabidopsis and targeted by the bacterium for parasitism.

Hypersensitive response and pathogenicity (hrp) genes control the ability of major groups of plant pathogenic bacteria to elicit the hypersensitive response (HR) in resistant plants and to cause disease in susceptible plants. A number of Hrp proteins share significant similarities with components of the type III secretion apparatus and flagellar assembly apparatus in animal pathogenic bacteria. Here we report that Pseudomonas syringae pv. tomato strain DC3000 (race 0) produces a filamentous surface appendage (Hrp pilus) of 6-8 nm in diameter in a solid minimal medium that induces hrp genes. Formation of the Hrp pilus is dependent on at least two hrp genes, hrpS and hrpH (recently renamed hrcC), which are involved in gene regulation and protein secretion, respectively. Our finding of the Hrp pilus, together with recent reports of Salmonella typhimurium surface appendages that are involved in bacterial invasion into the animal cell and of the Agrobacterium tumefaciens virB-dependent pilus that is involved in the transfer of T-DNA into plant cells, suggests that surface appendage formation is a common feature of animal and plant pathogenic bacteria in the infection of eukaryotic cells. Furthermore, we have identified HrpA as a major structural protein of the Hrp pilus. Finally, we show that a nonpolar hrpA mutant of P. syringae pv. tomato DC3000 is unable to form the Hrp pilus or to cause either an HR or disease in plants

▪ Abstract  Among many interesting and sophisticated mechanisms used by bacterial pathogens to subvert eukaryotic hosts is a class of specialized protein secretion systems (known as type III protein secretion systems) that deliver bacterial virulence proteins directly into the host cell. Recent studies have revealed four important features of these secretion systems. First, they are widespread among plant and animal bacterial pathogens, and mutations affecting type III protein secretion often eliminate bacterial virulence completely. Second, at least eight type III secretion components share sequence similarities with those of the flagellar assembly machinery and flagellum-like structures are associated with type III secretion, raising the possibility that these secretion systems are derived from the presumably more ancient flagellar assembly apparatus. Third, type III secretion is activated in vivo upon contact with host cells. Fourth, the type III secretion mechanism is Sec-independent and the effector proteins may possess mRNA-based targeting signals. This review highlights the similarities and differences among type III secretion systems of selected model plant and animal pathogenic bacteria.

The nonpathogenic bacteria Pseudomonas fluorescens and Escherichia coli can elicit a genotype hypersensitive response (HR) in plants if they express both the HR and pathogenesis (Hrp) protein secretion system and the HrpZ harpin from P. syringae pv syringae 61 and a P. syringae avirulence (avr gene whose presence is recognized by a corresponding disease resistance gene in the plant. We have found that the recognition event appears to require transfer of the Avr protein into the plant cell. Elicitation of a genotype-specific HR was observed with avrB+ P. fluorescens in soybean and Arabidopsis plants carrying resistance genes RPG1 and RPM1, respectively, and with avrPto+ E. coli in tomato plants carrying resistance gene PTO, but only if the Hrp secretion system, HrpZ, and the appropriate Avr proteins were produced in the same bacterial cell. The failure of avrB hyperexpression and exogenous AvrB or HrpZ to alleviate these requirements in soybean and Arabidopsis suggests that the site of AvrB action is not in the bacterial cell or plant apoplast. An Arabidopsis rps3 (rpm1) glabrous1 mutant was transformed with constructs expressing avrB and was crossed with and Arabidopsis ecotype Columbia (RPM1 GLABROUS1) plant. F1 seedlings (identified by their kanamycin-resistant, pubescent phenotype) exhibited extensive necrosis on cotyledon leaves 10 days postgermination. Ecotype Columbia and rps3-1 leaves biolistically compared with plasmids expressing the beta-glucuronidese (GUS) gene and avrB failed to produce GUS activity (indicative of cell death) only when RPM1 and avrB were present in the leaf. Thus, both stable and transient expression of avrB in Arabidopsis resulted in RPM1 dependent necrosis, and the only demonstrable site of action for AvrB inside plant cells

A proteinaceous elicitor of the plant defense reaction known as the hypersensitive response was isolated from Erwinia amylovora, the bacterium that causes fire blight of pear, apple, and other rosaceous plants. The elicitor, named harpin, is an acidic, heat-stable, cell-envelope-associated protein with an apparent molecular weight of 44 kilodaltons. Harpin caused tobacco leaf lamina to collapse and caused an increase in the pH of bathing solutions of suspension-cultured tobacco cells. The gene encoding harpin (hrpN) was located in the 40-kilobase hrp gene cluster of E. amylovora, sequenced, and mutated with Tn5tac1. The hrpN mutants were not pathogenic to pear, did not elicit the hypersensitive response, and did not produce harpin

An experimental investigation was undertaken to study low-energy electron exposure effects upon ZnO/K2SiO3 thermal control coating. The specimens were exposed to 10-, 30-, 50-, and 70-keV electrons, respectively. The spectral reflectance of each specimen was measured in situ before and after electron exposures. The solar absorptance was calculated by assuming a Johnson solar spectral irradiance distribution. Electron paramagnetic resonance and photoluminescence measurements were made before and after electron exposures to explain physical changes induced by the electron exposures. All the specimens exhibited a reflectance decrease throughout the visible and the near-infrared regions, and also the induced optical degradation was found to be electron energy dependent, with increased damage for increasing electron energy. It is believed that the optical degradation of ZnO/K2SiO3 thermal control coating, induced by the low-energy electron exposures, is mainly due to the ionization process of the ZnO pigment.