Plant intracellular immune receptors comprise a large number of multi-domain proteins resembling animal NOD-like receptors (NLRs). Plant NLRs typically recognize isolate-specific pathogen-derived effectors, encoded by avirulence (AVR) genes, and trigger defense responses often associated with localized host cell death. The barley MLA gene is polymorphic in nature and encodes NLRs of the coiled-coil (CC)-NB-LRR type that each detects a cognate isolate-specific effector of the barley powdery mildew fungus. We report the systematic analyses of MLA10 activity in disease resistance and cell death signaling in barley and Nicotiana benthamiana. MLA10 CC domain-triggered cell death is regulated by highly conserved motifs in the CC and the NB-ARC domains and by the C-terminal LRR of the receptor. Enforced MLA10 subcellular localization, by tagging with a nuclear localization sequence (NLS) or a nuclear export sequence (NES), shows that MLA10 activity in cell death signaling is suppressed in the nucleus but enhanced in the cytoplasm. By contrast, nuclear localized MLA10 is sufficient to mediate disease resistance against powdery mildew fungus. MLA10 retention in the cytoplasm was achieved through attachment of a glucocorticoid receptor hormone-binding domain (GR), by which we reinforced the role of cytoplasmic MLA10 in cell death signaling. Together with our data showing an essential and sufficient nuclear MLA10 activity in disease resistance, this suggests a bifurcation of MLA10-triggered cell death and disease resistance signaling in a compartment-dependent manner.

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Portions of the cuticle biosynthetic machinery originated in the last common ancestor of embryophytes and underwent evolution and diversification in land plants.

The aerial surface of higher plants is covered by a hydrophobic layer of cuticular waxes to protect plant tissues against enormous environmental challenges including the infection of various pathogens. As the first contact site between plants and pathogens, the layer of cuticular waxes could function as a plant physical barrier that limits the entry of pathogens, acts as a reservoir of signals to trigger plant defense responses, and even gives cues exploited by pathogens to initiate their infection processes. Past decades have seen unprecedented proceedings in understanding the molecular mechanisms underlying the biosynthesis of plant cuticular waxes and their functions regulating plant–pathogen interactions. In this review, we summarized the recent progress in the molecular biology of cuticular wax biosynthesis and highlighted its multiple roles in plant disease resistance against bacterial, fungal, and insect pathogens.

Powdery mildew caused by Blumeriagraminis f.sp. tritici (Bgt) seriously threatens the production of common wheat (Triticumaestivum L.). In eukaryotes, WD40-repeat (WDR) proteins usually participate in assembling protein complexes involved in a wide range of cellular processes. However, the potential function of WDR proteins in regulating crop resistance against biotrophic fungal pathogens, such as Bgt, remains unclear. In this study, we isolated TaHOS15, encoding a WDR protein, from wheat cultivar Jing411 and demonstrated that knockdown of TaHOS15 expression using virus- or transient-induced gene silencing attenuated wheat susceptibility to Bgt. The biochemical and molecular-biological assays revealed that TaHOS15 interacts with TaHDA6, a wheat homolog of Arabidopsis histone deacetylase AtHDA6, to constitute a transcriptional repressor complex. Furthermore, we defined the role of TaHOS15, which might act as an adaptor protein recruiting TaHDA6 to the chromatin of wheat defense-related genes including TaPR1, TaPR2, TaPR5, and TaWRKY45, where they repress histone acetylation. Moreover, reduced TaHOS15 or TaHDA6 transcript levels led to the decreased susceptibility to Bgt accompanied with the enhanced defense-related transcription under Bgt infection. Collectively, these results reveal that TaHOS15 functions in a histone deacetylase complex with TaHDA6 to fine-tune the defense response to Bgt in common wheat.

Environmental stresses such as salinity, drought, heat, freezing, heavy metal and even pathogen infections seriously threaten the growth and yield of important cereal crops including wheat and barley. There is growing evidence indicating that plants employ sophisticated epigenetic mechanisms to fine-tune their responses to environmental stresses. Here, we provide an overview of recent developments in understanding the epigenetic processes and elements—such as DNA methylation, histone modification, chromatin remodeling, and non-coding RNAs—involved in plant responses to abiotic and biotic stresses in wheat and barley. Potentials of exploiting epigenetic variation for the improvement of wheat and barley are discussed.

Wheat TaCDK8 interacts with TaWIN1 to regulate very-long-chain aldehyde biosynthesis required for efficient germination of Blumeria graminis f.sp. tritici. Powdery mildew caused by Blumeria graminis f.sp. tritici (Bgt) is a devastating disease of common wheat (Triticum aestivum L.). Bgt infection initiates with its conidia germination on the aerial surface of wheat. In this study, we isolated the cyclin-dependent kinase 8 (TaCDK8) from wheat cultivar Jing411 and found that silencing of TaCDK8 impeded Bgt germination. The biochemical and molecular-biological assays revealed that TaCDK8 interacts with and phosphorylates the wheat transcription factor wax inducer 1 (TaWIN1) to stimulate the TaWIN1-dependent transcription. Bgt conidia on the leaves of TaWIN1-silenced plants also showed reduced germination. Gas chromatographic analysis revealed that knockdown of TaCDK8 or TaWIN1 resulted in decreases of wax components and cutin monomers in wheat leaves. Moreover, Bgt germination on leaves of TaCDK8 or TaWIN1 silenced plants could be fully restored by application of wild-type cuticular wax. In vitro studies demonstrated that very-long-chain aldehydes absent from the cuticular wax of the TaCDK8 or TaWIN1 silenced plants were capable of chemically stimulating Bgt germination. These results implicated that the suppression of TaCDK8/TaWIN1 interaction negatively affects Bgt germination by interfering with very-long-chain aldehyde biosynthesis required for efficient fungal germination.

BackgroundNorcantharidin, the demethylated analog of cantharidin derived from a traditional Chinese medicine, Mylabris, has been used in the treatment of anti-cancer effects. However, the detailed mechanisms underlying this process are generally unclear. The aim of this study was to investigate the mechanism of NCTD-induced apoptosis in HepG2 cells.MethodsThe cytotoxicity was measured by MTT assay for cellular viability and by flow cytometry. The mitochondrial membrane potential and reactive oxygen species production was evaluated by flow cytometry analysis. The role of caspase activities were assayed using caspase apoptosis detection kit . Western blot analysis was used to evaluate the level of Cyto-C, Bcl-2, Bax, Bid, caspase 3, -9, -8 and PARP expressionResultsAfter treatment with NCTD, a decrease in the viability of HepG2 cells and increase in apoptosis were observed. NCTD-induced apoptosis was accompanied by an increase in ROS production, loss of mitochondrial membrane potential and release of cytochrome c(cyto-c) from the mitochondria to the cytosol and down-regulation of anti-apoptotic protein Bcl-2 levels with concurrent up-regulation in pro-apoptotic protein Bax levels. However, another pro-apoptotic molecule, Bid, showed no change in such same treatment. NCTD-increased activity of caspase 9,caspase 3 and the subsequent cleavage caspase substrate PARP were also observed. The expression levels of pro-caspase-8 were not changed after NCTD treatment.ConclusionThese results indicate that NCTD induced cytotoxicity in HepG2 cells by apoptosis, which is mediated through ROS generation and mitochondrial pathway.