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Plant pathogenic fungi and oomycetes employ sophisticated mechanisms for evading host recognition. After host penetration, many fungi and oomycetes establish a biotrophic interaction. It is assumed that different strategies employed by these pathogens to avoid triggering host defence responses, including establishment of biotrophic interfacial layers between the pathogen and host, masking of invading hyphae and active suppression of host defence mechanisms, are essential for a biotrophic parasitic lifestyle. During the infection process, filamentous plant pathogens secrete various effectors, which are hypothesized to be involved in facilitating effective host infection. Live-cell imaging of fungi and oomycetes secreting fluorescently labeled effector proteins as well as functional characterization of the components of biotrophic interfaces have led to the recent progress in understanding how eukaryotic filamentous pathogens evade plant recognition. [ABSTRACT FROM AUTHOR]

To cause rice blast disease, the fungus Magnaporthe oryzae produces biotrophic invasive hyphae that secrete effectors at the host–pathogen interface. Effectors facilitate disease development, but some (avirulence effectors) also trigger the host''s resistance gene-mediated hypersensitive response and block disease. The number of cloned M. oryzae avirulence effector genes has recently doubled, largely based on resequencing with a Japanese field isolate and association of avirulence activity with presence/absence polymorphisms in novel genes for secreted proteins. Effectors secreted by hyphae in rice cells accumulate in biotrophic interfacial complexes, and this property correlates with their translocation across plasma membrane into the rice cytoplasm. Interestingly, the translocated effectors moved into surrounding uninvaded cells, suggesting that effectors prepare host cells before the fungus enters them. [Copyright &y& Elsevier]

Recent findings demonstrate that cytoplasmic effectors from fungal and oomycete pathogens enter plant cells via clathrin-mediated endocytosis (CME). This raises several questions: Does effector secretion pathway facilitate host uptake? How is CME triggered in host cells? How are the effectors released from endosomal compartments to reach diverse subcellular destinations? [ABSTRACT FROM AUTHOR]

Insects secrete antimicrobial peptides as part of the innate immune response. Most antimicrobial peptides from insects have antibacterial but not antifungal activity. We have characterized an antifungal peptide, diapausin-1 from hemolymph of a lepidopteran insect, Manduca sexta (tobacco hornworm). Diapausin-1 was isolated by size exclusion chromatography from hemolymph plasma of larvae that were previously injected with a yeast, Saccharomyces cerevisiae . Fractions containing activity against S. cerevisiae were analyzed by SDS-PAGE and MALDI-TOF MS/MS and found to contain a 45-residue peptide that was encoded by sequences identified in M. sexta transcriptome and genome databases. A cDNA for diapausin-1 was cloned from cDNA prepared from fat body RNA. Diapausin-1 is a member of the diapausin family of peptides, which includes members known to have antifungal activity. The M. sexta genome contains 14 genes with high similarity to diapausin-1, each with 6 conserved Cys residues. Diapausin-1 was produced as a recombinant protein in Escherichia coli . Purified recombinant diapausin-1 was active against S. cerevisiae , with IC 50 of 12 μM, but had no detectable activity against bacteria. Spores of some plant fungal pathogens treated with diapausin-1 had curled germination tubes or reduced and branched hyphal growth. Diapausin-1 mRNA level in fat body strongly increased after larvae were injected with yeast or with Micrococcus luteus . In addition, diapausin-1 mRNA levels increased in midgut and fat body at the wandering larval stage prior to pupation, suggesting developmental regulation of the gene. Our results indicate that synthesis of diapausin-1 is part of an antifungal innate immune response to infection in M. sexta . [ABSTRACT FROM AUTHOR]

• We quantified the yield benefits of fungicide to wheat using plot and survey data. • Fungicide yield benefits (7.8 ± 15 %) were greater in wetter growing seasons. • Susceptible genotypes benefited more from fungicides (17 %) than resistant ones (6 %). • Fungicides improved stability and modified environment-adaptability of genotypes. • Fungicide yield benefits were greater (31 %) in the survey data. Foliar fungicides can account for a large portion of the yield gap in winter wheat (Triticum aestivum L.); however, their impacts on yield have been inconsistent in rainfed environments. We compiled a database of replicated field experiments and producer-reported fungicide and yield data from commercial fields to quantify the effects of fungicide application on winter wheat yield and yield stability. The database of field experiments (i.e., canopy level) included 56 non-inoculated environments spanning 12 growing seasons in eight Kansas locations, and was restricted to field experiments with direct comparisons between a foliar fungicide between Zadoks 40–55 and a side-by-side untreated control, resulting in 393 mean yield comparisons resulting from 3226 yield observations. The producer survey included genotype and fungicide management data from 654 commercial Kansas wheat fields cultivated across three growing seasons. Grain yield and weather conditions in the experimental and producer-reported database were similar, with seasonal precipitation ranging from ˜150 to 1035 mm and average grain yield of ˜3900 kg ha−1 with a ˜7000 kg ha−1 range. Foliar fungicide application resulted in 7.8 % average yield gain in the canopy-level data, ranging from −27 % to +97 %. Yield differences due to fungicide were strongly related to precipitation and to the ratio of precipitation and reference evapotranspiration (WS:WD) during the spring in the experimental data. Grain yield responsiveness to fungicide associated with the responsiveness of green canopy cover, kernel weight, biomass, and harvest index. Analysis of covariance suggested that grain yield usually decreased with increases in disease susceptibility in the absence of foliar fungicides; however, yield-disease relationships were either neutral or positive in the presence of fungicides. Average yield gain for resistant varieties was ˜166 kg ha−1 (5.6 %), which was lower than for intermediate (˜199 kg ha−1; 6.9 %) or susceptible genotypes (˜598 kg ha−1; 16.9 %). Foliar fungicides increased yield stability across genotypes at the canopy level and at the commercial field level. In the commercial-field level data, 53 % of the fields received foliar fungicide, with higher frequency in growing seasons with greater WS:WD (which were also higher yielding). The use of foliar fungicides was associated with improved yields and interacted with genotype's resistance level to stripe rust and with growing seasons' WS:WD. This work quantified and explained the yield benefits of foliar fungicide, and characterized its dependency on genotype-specific disease resistance and environmental conditions both at the canopy- and commercial field-levels. [ABSTRACT FROM AUTHOR]