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1.
Plant Physiol ; 193(4): 2806-2824, 2023 Nov 22.
Article in English | MEDLINE | ID: mdl-37706535

ABSTRACT

Pathogens compromise host defense responses by strategically secreting effector proteins. However, the molecular mechanisms by which effectors manipulate disease-resistance factors to evade host surveillance remain poorly understood. In this study, we characterized a Puccinia striiformis f. sp. tritici (Pst) effector Pst21674 with a signal peptide. Pst21674 was significantly upregulated during Pst infections in wheat (Triticum aestivum L.) and knocking down Pst21674 by host-induced gene silencing led to reduced Pst pathogenicity and restricted hyphal spread in wheat. Pst21674 interaction with the abscisic acid-, stress-, and ripening-induced protein TaASR3 was validated mainly in the nucleus. Size exclusion chromatography, bimolecular fluorescence complementation, and luciferase complementation imaging assays confirmed that TaASR3 could form a functional tetramer. Virus-induced gene silencing and overexpression demonstrated that TaASR3 contributes to wheat resistance to stripe rust by promoting accumulation of reactive oxygen species and cell death. Additionally, transcriptome analysis revealed that the expression of defense-related genes was regulated in transgenic wheat plants overexpressing TaASR3. Interaction between Pst21674 and TaASR3 interfered with the polymerization of TaASR3 and suppressed TaASR3-mediated transcriptional activation of defense-related genes. These results indicate that Pst21674 serves as an important virulence factor secreted into the host nucleus to impede wheat resistance to Pst, possibly by targeting and preventing polymerization of TaASR3.


Subject(s)
Basidiomycota , Triticum , Triticum/physiology , Transcription Factors/genetics , Transcription Factors/metabolism , Basidiomycota/physiology , Gene Silencing , Virulence/genetics , Plant Diseases/genetics
2.
Int J Mol Sci ; 24(4)2023 Feb 15.
Article in English | MEDLINE | ID: mdl-36835298

ABSTRACT

Low temperature is an important factor limiting plant growth. Most cultivars of Vitis vinifera L. are sensitive to low temperatures and are at risk of freezing injury or even plant death during winter. In this study, we analyzed the transcriptome of branches of dormant cv. Cabernet Sauvignon exposed to several low-temperature conditions to identify differentially expressed genes and determine their function based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG)enrichment analyses. Our results indicated that exposure to subzero low temperatures resulted in damage to plant cell membranes and extravasation of intracellular electrolytes, and that this damage increased with decreasing temperature or increasing duration. The number of differential genes increased as the duration of stress increased, but most of the common differentially expressed genes reached their highest expression at 6 h of stress, indicating that 6 h may be a turning point for vines to tolerate extreme low temperatures. Several pathways play key roles in the response of Cabernet Sauvignon to low-temperature injury, namely: (1) the role of calcium/calmodulin-mediated signaling; (2) carbohydrate metabolism, including the hydrolysis of cell wall pectin and cellulose, decomposition of sucrose, synthesis of raffinose, and inhibition of glycolytic processes; (3) the synthesis of unsaturated fatty acids and metabolism of linolenic acid; and (4) the synthesis of secondary metabolites, especially flavonoids. In addition, pathogenesis-related protein may also play a role in plant cold resistance, but the mechanism is not yet clear. This study reveals possible pathways for the freezing response and leads to new insights into the molecular basis of the tolerance to low temperature in grapevine.


Subject(s)
Freezing , Gene Expression Regulation, Plant , Transcriptome , Vitis , Gene Expression Profiling , Plant Proteins/genetics , Signal Transduction , Vitis/genetics
3.
Micromachines (Basel) ; 13(8)2022 Jul 25.
Article in English | MEDLINE | ID: mdl-35893172

ABSTRACT

A tri-axis accelerometer with a digital readout circuit and communication system is introduced. It is composed of two resonant accelerometers in the x and y-axis, and a seesaw capacitive one in the z-axis. The device is encapsulated in air to ensure that the z-axis works in an over-damped state. Moreover, the closed-loop drive circuit establishes the x-axis and y-axis in resonant mode, and the z-axis in force balance mode. A miniaturized measurement based on FPGA is designed to collect these output signals. The phase noise of the resonance part and the amplitude noise of the seesaw part are studied by simulation. The model can predict the contribution of each part to the measurement error and Allan variance. Multiplied clock and Kalman filter in sliding window are used to reduce the frequency error. The test results show that the accelerometer has low bias instability (<30 µg), low cross-coupling error (<0.5%), and low nonlinearity (<0.1%). The tri-axis digital accelerometer with serial ports is more valuable than the previous works with large commercial instruments.

4.
New Phytol ; 236(1): 266-282, 2022 10.
Article in English | MEDLINE | ID: mdl-35729085

ABSTRACT

Sugar efflux from host plants is essential for pathogen survival and proliferation. Sugar transporter-mediated redistribution of host sugar contributes to the outcomes of plant-pathogen interactions. However, few studies have focused on how sugar translocation is strategically manipulated during host colonization. To elucidate this question, the wheat sugar transport protein (STP) TaSTP3 responding to Puccinia striiformis f. sp. tritici (Pst) infection was characterized for sugar transport properties in Saccharomyces cerevisiae and its potential role during Pst infection by RNA interference and overexpression in wheat. In addition, the transcription factors regulating TaSTP3 expression were further determined. The results showed that TaSTP3 is localized to the plasma membrane and functions as a sugar transporter of hexose and sucrose. TaSTP3 confers enhanced wheat susceptibility to Pst, and overexpression of TaSTP3 resulted in increased sucrose accumulation and transcriptional suppression of defense-related genes. Furthermore, TaWRKY19, TaWRKY61 and TaWRKY82 were identified as positive transcriptional regulators of TaSTP3 expression. Our findings reveal that the Pst-induced sugar transporter TaSTP3 is transcriptionally activated by TaWRKY19/61/82 and facilitates wheat susceptibility to stripe rust possibly through elevated sucrose concentration, and suggest TaSTP3 as a strong target for engineering wheat resistance to stripe rust.


Subject(s)
Basidiomycota , Triticum , Basidiomycota/physiology , Gene Expression Regulation, Plant , Plant Diseases , Sucrose/metabolism , Sugars/metabolism , Transcription Factors/metabolism , Triticum/genetics , Triticum/metabolism
6.
Environ Microbiol ; 20(11): 4037-4050, 2018 11.
Article in English | MEDLINE | ID: mdl-30307098

ABSTRACT

The early development of a rust fungus is dependent on the endogenous lipids stored in the urediniospores. After it establishes a parasitic relationship with the host, sugars absorbed from the host cells by haustoria become the primary nutrients. The tricarboxylic acid (TCA) cycle is essential to oxidize these nutrients. However, few studies have addressed the role of citrate synthase (CS), a rate-limiting enzyme of the TCA cycle, during the infection process of rust fungi. In this study, a CS gene from Puccinia striiformis f. sp. tritici (Pst), PsCS1, was cloned and characterized. Transcripts of PsCS1 and the enzyme activity of the CS were increased in the early Pst infection stage. Biochemical features and subcellular localization revealed that PsCS1 encoded a mitochondrial CS. Size exclusion chromatography, yeast two-hybrid and bimolecular fluorescence complementation experiments confirmed that PsCS1 could form a functional homo-octamer. The overexpression of PsCS1 enhanced the resistance of Escherichia coli to salt stress. The knockdown of PsCS1 using a host-induced gene silencing (HIGS) system blocked Pst growth in wheat. These results indicate that PsCS1 is required for nutrient metabolism in Pst and contributes to Pst infection by regulating ATP production and the supply of carbon sources.


Subject(s)
Basidiomycota/enzymology , Citrate (si)-Synthase/metabolism , Fungal Proteins/metabolism , Plant Diseases/microbiology , Triticum/microbiology , Adenosine Triphosphate/metabolism , Basidiomycota/genetics , Basidiomycota/pathogenicity , Citrate (si)-Synthase/genetics , Fungal Proteins/genetics , Gene Silencing , Mitochondria/enzymology , Mitochondria/genetics , Protein Isoforms/genetics , Protein Isoforms/metabolism , Virulence
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