The model systems used in the lab

The model system Ustilago maydis

Ustilago maydis is a dimorphic fungus, which belongs to the Basidiomycota. It is long known that U. maydis is the causal agent of corn smut disease in maize and is considered to be amongst the 5 most devastating plant pathogens world-wide1. Due to its genetic tractability U. maydis became a powerful model system in molecular plant pathology research2,3,4,5. In cell culture U. maydis grows as a yeast-like cell (named sporidium), but at the beginning of its pathogenic life-cycle the fungus undergoes a morphogenic transition and begins to grow as a filamentous hypha (Figure 1). Upon initiation of the infection, two yeast-like cells recognize each other and fuse in order to form another type of hypha that is able to invade maize tissue. This subsequently results in so-called tumours in stem, leaves and flowers (Figure 2). Interestingly, these U. maydis-induced tumours are known as a Mexican a delicacy, named 'cuitlachoche'. Nowadays fungicides efficiently control U. maydis infections. However, depending on climatic conditions infections can lead to significant grain-yield loss. Moreover, this pathogen is listed as a potential bio-weapon by the Ad Hoc Group of the Biological Weapons Convention of the United States of America6.

U. maydis is not only a pathogen; it has also a long-standing history as a model system for analyzing DNA recombination and repair. The famous 'Holliday junction' for DNA recombination was discovered in U. maydis7. In addition, we recently demonstrated the utility of this fungus as a more general model system for fundamental cell biology8. Our work has shown that U. maydis cells contain a prominent microtubule cytoskeleton and that the basic machinery for hyphal growth is reminiscent of that of mammalian neurons. In addition, this fungus undergoes an open mitosis that is mainly supported by the motor protein dynein9. Furthermore, a genome wide comparison of the predicted proteome revealed that U. maydis shares more proteins with humans than with the budding yeast Saccharomyces cerevisiae.

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1 Fisher et al (2012), Nature, 484:186.
2 Banuett, F. (1995), Annu Rev Genet, 29:179.
3 Feldbrügge et al (2004), Curr Opin Microbiol, 7:666.
4 Perez-Martin (2006), Mol Genet Genomics, 276:211.
5 Bölker M. (2001), Microbiology, 147:1395.
6 Madden & Wheelis (2003), Annu. Rev. Phytopathol, 41:155.
7 Holliday, R. (2004), DNA Repair, 3:671.
8 Steinberg and Perez-Martin (2008), Trends Cell Biol, 18:61.
9 Straube et al (2005), EMBO J, 24:1674.

The wheat pathogen Mycosphaerella graminicola

M. graminicola is a dimorphic Ascomycete (Figure 3) that causes Septoria blotch disease, which is the most serious diseases of wheat in Europe. Wheat is one of the three major cereals grown worldwide and it is of central importance to secure food supply for a growing world population. However, yield losses as a result of fungal disease is estimated to be a major challenge, which is indicated by ∼20% of the Australian wheat harvest lost between 1998 and 2008, and up to 10% losses in the UK1,2. M. graminicola (Septoria tritici) is the most common foliar disease of winter wheat, affecting 73% of crops sampled (UK Disease and Pest Incidence Reports). In Europe, M. graminicola causes up 40% yield loss and is therefore considered the most devastating wheat pathogen in Western Europe3 and in particular in the UK4, where the annual financial loss already reached £50 million (Rothamsted Research-Fungicide Resistance Report 2009).

An increasing number of molecular tools for working with M. graminicola are available5,6, including in vivo labelling of proteins using GFP (Figure 4). Having these tools in hand allows us to investigate the molecular basis of pathogenicity in this severe pathogen. In collaboration with Syngenta Crop Science, my laboratory has started to investigate the role of the fungal specific myosin XVII secretion pathway in development and pathogenicity of M. graminicola.

1 Murray and Brennan (2009), Austral. Plant Pathol, 38:558.
2 King et al (1983), Ann Appl Biol, 103:345.
3 Kema et al (2002), Genetics, 161:1497.
4 Hardwick et al (2001), Plant Pathol, 50:453.
5 Zwiers and De Waard (2001), Curr. Genet, 39:388.
6 Bowler et al (2010), Mol Plant Pathol, 11:691.

Pathogenic life cycle of U. maydis

Figure 1: Pathogenic life cycle of U. maydis. Yeast-like cells life in soil and are saprotrophic, but switch to filamentous growth upon initiation of the pathogenic cycle. Sporulation and subsequent meiosis requires infection of the maize plant (image taken from Steinberg and Perez-Martin, 2008, Trends Cell Biol. 18:61).

Symptoms of corn smut disease caused by Ustilago maydis

Figure 2: Symptoms of corn smut disease caused by Ustilago maydis (right image from Brefeld 1983, Untersuchungen aus dem Gesamtgebiet der Mykologie. 5, 67). Bar is given in micrometers; left images: (Steinberg lab, unpublished).

Morphology of the dimorphic wheat pathogen

Figure 3: Morphology of the dimorphic wheat pathogen Mycosphaerella graminicola (anamorph: Septoria tritci). Bar is given in micrometers (Steinberg lab, unpublished).

Localisation of a myosin-chitin synthase fused to AcGFP (Mg_Mcs1)

Figure 4: Localisation of a myosin-chitin synthase fused to AcGFP (Mg_Mcs1) in M. graminicola. Dotted line in the inset indicates area of intensity measurement, given in the linescan profile. Bar is given in micrometres (unpublished data, Steinberg lab).