Program Book - 27th Fungal Genetics Conference

CONCURRENT SESSION ABSTRACTSSaturday, March 16 2:00 PM–5:00 PMMerrill HallParallels between Fungal Pathogens of Plants and AnimalsCo-chairs: Barbara Howlett and Axel BrakhageEmerging fungal (and Oomycete) threats to plant and ecosystem health. Sarah J. Gurr 1* , Daniel Bebber 1 , Matthew Fisher 2 . 1) Plant Sciences, OxfordUniversity, Oxford, Oxfordshire; 2) Imperial College of Science, Technology and Medicine, London.Fungal diseases have increased in severity and scale since the mid 20th Century and now pose a serious challenge to global food security and ecosystemhealth (Gurr et al., 2011 Fungal Biology Reviews 25 181-188 ). We have demonstrated recently that the threat to plants of fungal infection has nowreached a level that outstrips that posed by bacterial and viral diseases combined (Fisher et al., 2012 Nature 484 185-194) I shall highlight some of themore notable fungal and oomycete plant diseases and will draw attention to the emergence of new pathotypes affecting crop yields and decimating ournatural and managed landscapes. We have calculated that the losses due to persistent disease (that is, non-epidemic) caused by, for example rice blast,wheat stem rust, corn smut, soybean rust and potato late blight, if mitigated, would be sufficient to feed 8.5% of the global population (based on 2000calories per day for 1 year). Moreover, tree losses due to fungal and oomycete diseases such as dutch elm, chestnut blight, sudden oak death, jarrah diebackand pine beetle/blue stain fungus, thus far, have been estimated to account for significant CO2 sequestration losses (Fisher et al., 2012). The spreadof such organisms around the world is facilitated primarily by trade, but there is increasing concern that climate change may allow their establishment inregions hitherto deemed unsuitable. Increasing latitudinal ranges are anticipated under rising temperatures. However, the interactions between climatechange, crops and natural enemies are complex, and the extent to which crop pests and pathogens have altered their latitudinal ranges in response toglobal warming is largely unknown. We can demonstrate, from thousands of observations of hundreds of pests and pathogens, their shift polewards since1950, with a more rapid shift since 1990 (Bebber et al., (under review)). This latitudinal shift is seen in both Hemispheres. Moreover, the rate of movementsince 1950 is identical to that predicted by global climate data. This observed trend cannot be explained by latitudinal variation in technical capacity todetect and report pest incidences.Melanin as virulence determinant of human and plant pathogenic fungi. Axel A. Brakhage, Andreas Thywissen, Juliane Macheleidt, Sophia Keller, VitoValiante, Thorsten Heinekamp. Molec & Appl Microbiology, Leibniz Inst Natural Prod Res Infection Biol-HKI, Jena, Germany.In fungi, melanins are often associated with the cell wall and also contribute to the structural rigidity of spores. In several plant and human pathogenicfungi, melanins contribute to pathogenicity. For example, pigmentless mutants of the plant pathogens Magnaporthe oryzae and Colletotrichumlagenarium, as well as the human-pathogenic fungi Cryptococcus neoformans and Aspergillus fumigatus are less virulent when compared to melaninproducingwild-type strains. In M. oryzae, it was shown that a 1,8-dihydroxynaphthalene (DHN) melanin layer between the cell wall and the cell membraneis essential for turgor generation. The melanin acts as a barrier to the efflux of solute from the appressorium, which occurs as pressure is generated.Cellular turgor is translated into mechanical force of infection hyphae, forcing it through the leaf cuticle (1) . In human-pathogenic fungi, high turgor pressureis not required for penetration of tissue. In these fungi, melanin displays other virulence attributes such as the scavenging of reactive oxygen species. In A.fumigatus, at least two types of melanin are produced: Pyomelanin by polymerization of homogentisic acid, and DHN melanin. Transcription of genesessential for pyomelanin and DHN-melanin biosynthesis is detected during infection of mice. However, pyomelanin seems to be dispensable for fungalvirulence in the murine infection models tested (2,3) . DHN melanin is responsible for the grey-green color of A. fumigatus conidia. The biosynthesis enzymesof DHN melanin are encoded by six genes. Centrally is the polyketide synthase gene pksP, whose deletion results in a mutant strain with drasticallyattenuated virulence. Recent data of our laboratory showed that DHN melanin is essential not only for inhibition of apoptosis of phagocytes by interferingwith the host PI3K/Akt signaling cascade but also for effective inhibition of acidification of conidia-containing phagolysosomes (4,5) . These features allow A.fumigatus to survive in phagocytes and thereby to escape from human immune effector cells and to become an aggressive pathogen. 1) Wilson RA &Talbot NJ (2009) Nat Rev Microbiol. 7: 185-195 2) Keller et al. (2011) PLoS One 6:e26604 3) Schmaler-Ripcke et al. (2009) Appl Environ Microbiol. 75: 493 4)Thywiben et al. (2011) Front Microbiol. 2: 96 5) Volling et al. (2011) Cell Microbiol. 13: 1130.Nutrient immunity and systemic readjustment of metal homeostasis modulate fungal iron availability during the development of renal infections.Joanna Potrykus 1 , David Stead 2 , Dagmar S Urgast 3 , Donna MacCallum 1 , Andrea Raab 3 , Jörg Feldmann 3 , Alistair JP Brown 1 . 1) Aberdeen Fungal Group,University of Aberdeen, Aberdeen, United Kingdom; 2) Aberdeen Proteomics, University of Aberdeen, Aberdeen, United Kingdom; 3) Trace ElementSpeciation Laboratory, University of Aberdeen, Aberdeen, United Kingdom.Iron is a vital micronutrient that can limit the growth and virulence of many microbial pathogens. Here we show, that in the murine model ofdisseminated candidiasis, the dynamics of iron availability are driven by a complex interplay of localized and systemic events. As the infection progresses inthe kidney, Candida albicans responds by broadening its repertoire of iron acquisition strategies from non-heme iron (FTR1-dependent) to heme-ironacquisition (HMX1-dependent), as demonstrated in situ by laser capture microdissection, RNA amplification and qRT-PCR. This suggested changes in ironavailability in the vicinity of fungus. This was confirmed by 56 Fe iron distribution mapping in infected tissues via laser ablation-ICP-MS, which revealeddistinct iron exclusion zones around the lesions. These exclusion zones correlated with the immune infiltrates encircling the fungal mass, and wereassociated with elevated concentrations of murine heme oxygenase (HO-1) circumventing the lesions. Also, MALDI Imaging revealed an increase in hemeand hemoglobin alpha levels in the infected tissue, with their distribution roughly corresponding to that of 56 Fe. Paradoxically, whilst iron was excludedfrom lesions, there was a significant increase in the levels of iron in the kidneys of infected animals. This iron appeared tissue bound, was concentratedaway from the fungal exclusion zones, and was accompanied by increased levels of ferritin and HO-2. This iron accumulation in the kidney correlated withdefects in red pulp macrophage function and red blood cell recycling in the spleen, brought about by the fungal infection. Significantly, this effect could bereplicated by selective chemical ablation of splenic red pulp macrophages by clodronate. Collectively, our data indicate that systemic events shapemicronutrient availability within local tissue environments during fungal infection. The infection attenuates the functionality of splenic red pulpmacrophages leading to elevated renal involvement in systemic iron homeostasis and increased renal iron loading. Simultaneously, localized nutrientimmunity limits iron availability around foci of fungal infection in the kidney. In response, the fungus modulates its iron assimilation strategies.84