Morphology-controlled growth of ZnO nano-and microstructures was achieved by microwave irradiation. Various basic ZnO structures, including nanorods, nanocandles, nanoneedles, nanodisks, nanonuts, microstars, microUFOs, and microballs were simply synthesized at a low temperature (90 °C) with low power microwaveassisted heating (about 50 W) and a subsequent aging process. These results could be obtained by changing the precursor chemicals, the capping agents, and the aging times. Even more complex ZnO structures, including ZnO bulky stars, cakes, and jellyfishes, were constructed by microwave irradiation to a mixture of the asprepared basic ZnO structures and the solution I, IV, or V. This is a fast, simple, and reproducible method which does not require any template, catalyst, or surfactant but can control the morphology of ZnO crystals from simple to complex. Scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy dispersive X-ray spectroscopy (EDX), and X-ray diffraction (XRD) were used to observe the morphology, crystallinity, and chemical composition of the ZnO structures. Growth mechanisms for shapeselective ZnO synthesis were proposed based on these results.

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Ascochyta blight in chickpea (Cicer arietinum L.) is a devastating fungal disease caused by the necrotrophic pathogen, Ascochyta rabiei (Pass.) Lab. To elucidate the genetic mechanism of pathotype-dependent blight resistance in chickpea, F 7 -derived recombinant inbred lines (RILs) from the intraspecific cross of PI 359075(1) (blight susceptible) × FLIP84-92C(2) (blight resistant) were inoculated with pathotypes I and II of A. rabiei. The pattern of blight resistance in the RIL population varied depending on the pathotype of A. rabiei. Using the same RIL population, an intraspecific genetic linkage map comprising 53 sequence-tagged microsatellite site markers was constructed. A quantitative trait locus (QTL) for resistance to pathotype II of A. rabiei and two QTLs for resistance to pathotype I were identified on linkage group (LG)4A and LG2+6, respectively. A putative single gene designated as Ar19 (or Ar21d) could explain the majority of quantitative resistance to pathotype I. Ar19 (or Ar21d) appeared to be required for resistance to both pathotypes of A. rabiei, and the additional QTL on LG4A conferred resistance to pathotype II of A. rabiei. Further molecular genetic approach is needed to identify individual qualitative blight resistance genes and their interaction for pathotype-dependent blight resistance in chickpea.

Fusarium head blight (FHB) of barley (Hordeum vulgare L.) is caused by Fusarium graminearum. FHB causes yield losses and reduction in grain quality primarily due to the accumulation of trichothecene mycotoxins such as deoxynivalenol (DON). To develop an understanding of the barley-F. graminearum interaction, we examined the relationship among the infection process, DON concentration, and host transcript accumulation for 22,439 genes in spikes from the susceptible cv. Morex from 0 to 144 h after F. graminearum and water control inoculation. We detected 467 differentially accumulating barley gene transcripts in the F. graminearum-treated plants compared with the water control-treated plants. Functional annotation of the transcripts revealed a variety of infection-induced host genes encoding defense response proteins, oxidative burst-associated enzymes, and phenylpropanoid pathway enzymes. Of particular interest was the induction of transcripts encoding potential trichothecene catabolic enzymes and transporters, and the induction of the tryptophan biosynthetic and catabolic pathway enzymes. Our results define three stages of E graminearum infection. An early stage, between 0 and 48 h after inoculation (hai), exhibited limited fungal development, low DON accumulation, and little change in the transcript accumulation status. An intermediate stage, between 48 and 96 hai, showed increased fungal development and active infection, higher DON accumulation, and increased transcript accumulation. A majority of the host gene transcripts were detected by 72 hai, suggesting that this is an important timepoint for the barley-F. graminearum interaction. A late stage also identified between 96 and 144 hai, exhibiting development of hyphal mats, high DON accumulation, and a reduction in the number of transcripts observed. Our study provides a baseline and hypothesis-generating dataset in barley during F. graminearum infection and in other grasses during pathogen infection.

We report a method for synthesizing exposed crystal face controlled 3D ZnO superstructures under mild conditions (at room temperature or 90 degrees C under 1 atm) without organic additives. The exposed crystal faces of the building blocks of the 3D structures were controlled by varying the reactant concentrations and the reaction temperatures. On the basis of the experimental results, we speculated a possible mechanism for the formation of the four distinct 3D ZnO superstructures (structures I, II, III, and IV) under the different growth conditions. The optical properties of the 3D ZnO superstructures were probed by UV-vis diffuse reflectance spectroscopy. The spectra were shifted depending on the dimensions and sizes of the building blocks of the 3D superstructures. The photocatalytic activities of the 3D superstructures varied according to the exposed crystal faces, which could be controlled by this method (structure I > structure IV > structure III > structure II).

We report the synthesis of carbon-doped zinc oxide nanostructures using vitamin C, and their visible light photocatalytic activity. Amorphous/crystalline vitamin C-ZnO (VitC-ZnO) structures were obtained from a solution of zinc nitrate hexahydrate, HMT, and vitamin C through heating at 95 C for 1 h. VitC-ZnO structures were calcined in air at 500 C for 2 h to create C-doped ZnO nanostructures. Calcined structures were polycrystalline, with an average crystal domain size of 7 nm. EDS, XPS, and XRD analysis revealed the substitution of oxygen with carbon and the formation of Zn-C bonds in the C-doped ZnO nanostructures. The carbon concentrations, in the form of carbide, were controlled by varying the concentrations of vitamin C (more than 1 mM) added to reaction solutions. On the basis of these experimental results, we propose a possible formation mechanism for C-doped ZnO nanostructures. The C-doped ZnO nanostructures exhibited visible light absorption bands that were red-shifted relative to the UV exciton absorption of pure ZnO nanostructures. The visible light (l $ 420 nm) photocatalytic activities of C-doped ZnO nanostructures were much better than the activities of pure ZnO nanostructures.

Fusarium head blight, caused primarily by Fusarium graminearum, is a major disease problem on barley (Hordeum vulgare L.). Trichothecene mycotoxins produced by the fungus during infection increase the aggressiveness of the fungus and promote infection in wheat (Triticum aestivum L.). Loss-of-function mutations in the TRI5 gene in F. graminearum result in the inability to synthesize trichothecenes and in reduced virulence on wheat. We examined the impact of pathogen-derived trichothecenes on virulence and the transcriptional differences in barley spikes infected with a trichothecene-producing wild-type strain and a loss-of-function tri5 trichothecene nonproducing mutant. Disease severity, fungal biomass, and floret necrosis and bleaching were reduced in spikes inoculated with the tri5 mutant strain compared with the wild-type strain, indicating that the inability to synthesize trichothecenes results in reduced virulence in barley. We detected 63 transcripts that were induced during trichothecene accumulation, including genes encoding putative trichothecene detoxification and transport proteins, ubiquitination-related proteins, programmed cell death-related proteins, transcription factors, and cytochrome P450s. We also detected 414 gene transcripts that were designated as basal defense response genes largely independent of trichothecene accumulation. Our results show that barley exhibits a specific response to trichothecene accumulation that can be separated from the basal defense response. We propose that barley responds to trichothecene accumulation by inducing at least two general responses. One response is the induction of genes encoding trichothecene detoxification and transport activities that may reduce the impact of trichothecenes. The other response is to induce genes encoding proteins associated with ubiquitination and cell death which may promote successful establishment of the disease.

We have studied the precursor effects of citric acid and various citrates-including triethyl citrate, tripotassium citrate, trisodium citrate and triammonium citrate-on the formation of ZnO crystals in alkaline solution. These citrate-related chemicals could be divided into three groups (group A, triethyl citrate; group B, tripotassium citrate and trisodium citrate; and group C, citric acid and triammonium citrate) based on their activity for modifying the ZnO growth direction and solution pH dependency on their concentration. We could obtain ZnO structures with various distinct morphologies by simply changing the concentration of citric acid or citrate additive dissolved in the alkaline reaction solution. On the basis of the results, we propose the growth mechanisms underlying the formation of the various ZnO structures in the absence and presence of citric acid or citrate additives.