50 research outputs found

    Beheersing van valse meeldauw in Impatiens

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    De éénjarige zomerbloeier Impatiens walleriana vormt een belangrijk onderdeel in het assortiment van perkgoed. Ondermeer in 2007 waren er door de natte weersomstandigheden grote problemen met uitval door valse meeldauw in de consumentfase. Hierdoor kwam de vraag of er tijdens de opkweek niet meer preventieve maatregelen genomen kunnen worden om infectie door valse meeldauw onder vochtige omstandigheden te verminderen of te voorkomen. Daarnaast was het onbekend of de besmetting met valse meeldauw op Nederlandse locaties veroorzaakt wordt door één soort of meerdere soorten. In een literatuurstudie is alle beschikbare informatie over valse meeldauw en mogelijkheden voor beheersen/ bestrijding samengeva

    Voorkomen van uitval bij Impatiens walleriana onder veldcondities

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    Abstract Wageningen UR Greenhouse Horticulture, together with Syngenta Seeds performed field trials with fungicides and fertilizing products to prolong the consumer value of Impatiens walleriana (busy lily). This project was funded by the Dutch Horticultural Board. The plants were situated on two field locations, both in the field and in pots to follow the natural disease development with and without interaction with soil pathogens (e.g. downy mildew). The results of this study show that Ridomil Gold is effective against early infestation from soil propagules of downy mildew, but there is no effectivity against leaf infections. Products based on phoshite (potassium phosphite, product X of Everris) slow down the infection process with a few weeks. Especially, later in the season when the conidia are most dominantly present. It is recommended to screen multiple products which are effective against resting spores of downy mildew. Sensitive Impatiens species should preferably be planted early in the season and not directly in soil with high risk of surviving propagules

    Nieuwe middelen tegen valse meeldauw in Impatiens walleriana

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    Abstract Wageningen UR Greenhouse Horticulture, together with Syngenta Seeds tested various combinations of agents for their effects to increase plant defense against infection of downy mildew in the consumer phase. All means were dosed 2-3 times during the growers phase. There are three new products, which were found to strengthen Impatiens plants against infection by downy mildew. It is still unclear how these products can be combined with other agents that also control pathogenic soil fungi so that failure occurs less rapidly under field conditions at high disease pressure. In 2011, this research will be continued at two field locations

    The rice NLR pair Pikp-1/Pikp-2 initiates cell death through receptor cooperation rather than negative regulation

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    Plant NLR immune receptors are multidomain proteins that can function as specialized sensor/helper pairs. Paired NLR immune receptors are generally thought to function via negative regulation, where one NLR represses the activity of the second and detection of pathogen effectors relieves this repression to initiate immunity. However, whether this mechanism is common to all NLR pairs is not known. Here, we show that the rice NLR pair Pikp-1/Pikp-2, which confers resistance to strains of the blast pathogen Magnaporthe oryzae (syn. Pyricularia oryzae) expressing the AVR-PikD effector, functions via receptor cooperation, with effector-triggered activation requiring both NLRs to trigger the immune response. To investigate the mechanism of Pikp-1/Pikp-2 activation, we expressed truncated variants of these proteins, and made mutations in previously identified NLR sequence motifs. We found that any domain truncation, in either Pikp-1 or Pikp-2, prevented cell death in the presence of AVR-PikD, revealing that all domains are required for activity. Further, expression of individual Pikp-1 or Pikp-2 domains did not result in cell death. Mutations in the conserved P-loop and MHD sequence motifs in both Pikp-1 and Pikp-2 prevented cell death activation, demonstrating that these motifs are required for the function of the two partner NLRs. Finally, we showed that Pikp-1 and Pikp-2 associate to form homo- and hetero-complexes in planta in the absence of AVR-PikD; on co-expression the effector binds to Pikp-1 generating a tri-partite complex. Taken together, we provide evidence that Pikp-1 and Pikp-2 form a fine-tuned system that is activated by AVR-PikD via receptor cooperation rather than negative regulation

    Structure-Function Analysis of Barley NLR Immune Receptor MLA10 Reveals Its Cell Compartment Specific Activity in Cell Death and Disease Resistance

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    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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