http://www.canolacouncil.org/clubroot/resources.aspx, http://tu-dresden.de/die_tu_dresden/fakultaeten/fakultaet_mathematik_und_naturwissenschaften/fachrichtung_biologie/botanik/pflanzenphysiologie/clubroot, http://www.ohio.edu/people/braselto/plasmos/

Fusarium asiaticum is the predominant causal agent of Fusarium head blight (FHB) in southern China. The genetic diversity was assessed by analyzing 448 single-spore F. asiaticum isolates from 18 sampling sites that were 10 to 2,000 km apart, using seven highly informative variable number of tandem repeat (VNTR) markers. This analysis showed a significant degree of population subdivision (P < 0.001) among populations from upper, middle, and lower valleys of the Yangtze River, with little gene flow (Nm = 1.210). We observed a strong association between this genetic population subdivision and the mycotoxin produced. Our results show that the dramatic cline in trichothecene chemotypes may be explained by a recent and significant invasion of 3-acetyldeoxynivalenol (3ADON) producers in FHB pathogen composition in the middle valley. Using Bayesian statistics, we found a biased gene flow from 3ADON to nivalenol (NIV) populations. In addition, we observed significant genetic differentiation and linkage disequilibrium between NIV- and 3ADON-producing isolates at the same sampling sites. The impact of the changed agronomy and trade of cereal commodities on the spread of the new Fusarium population and the consequent increase of FHB observed in southern China are discussed.

No abstract

This study identifies several novel susceptibility genes for MMD. The association with homocysteine metabolism and the immune system enrichment of susceptibility gene expression suggest that therapeutic interventions targeting these pathways may be effective approaches for MMD treatment.

To acquire iron from plant hosts, fungal pathogens have evolved at least two pathways for iron uptake. One system is hinged on the secretion and subsequent uptake of low-molecular-weight iron chelators termed siderophores, while the other uses cell-surface reductases to solubilize ferric iron by reducing it to ferrous iron for uptake. We identified five iron uptake-related genes from the head blight pathogen Fusarium graminearum and showed that they were transcribed in response to iron limitation. To examine the relative contribution of the reductive and siderophore pathways of iron uptake, we created mutants disrupted at the ferroxidase gene FET3 (Deltafet3) or the siderophore biosynthetic gene SID1 (Deltasid1). The Deltafet3 mutants produced wild-type amounts of siderophores and grew at the same rate as the wild-type under iron limitation, but accumulated high levels of free intracellular iron. The Deltasid1 mutants did not produce siderophores and grew slowly under low iron conditions. Transcription of the iron uptake-related genes was induced in the Deltasid1 mutant regardless of the growth medium iron content, whereas these genes were transcribed normally in the Deltafet3 mutant. Finally, the Deltasid1 mutants could infect single, inoculated spikelets, but were unable to spread from spikelet-to-spikelet through the rachises of wheat spikes, while the Deltafet3 mutants behaved as wild-type throughout infection. Together, our data suggest that siderophore-mediated iron uptake is the major pathway of cellular iron uptake and is required for full virulence in F. graminearum.