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A Microbial Biorealm page on the genus Ustilago

Fig1. Image of U. maydis on corn. The white and grey fungus is consumed in a recipe called huitlacoche. (


Higher order taxa

Eukaryota; Fungi; Basidiomycota; Ustilaginomycetes; Ustilaginomycetidae; Ustilaginales; Ustilaginaceae; Ustilago


Ustilago maydis (zeae is obsolete name), U. scitaminea (cane smut), U. lituana (grass smut), U. violacea, U. scabiosae, U. utriculosae, U. sphaerogena, U. bullata, U. nigra, U. hordei, U. heterogena

Description and significance

There are approximately 850 species of smut fungi. Their name came about from the dark brown or black loosely filled sori on the affected plant. In all cases the smuts produce the sori on the vegetative organs of the plant (Moore-Landecker, 1996). Ustilago maydis is a type of yeast that inhabits dead soil or plant environments. It is known as a dimorphic fungus because it can grow in two manners; one is the single-celled form on dead plants and the other is a filamentous mycelial form during the invasion of a plant and also during mating. Typically it can most often be found affecting sweet corn (CWBInfo, 1999-2001). The most prominent feature of its infection on corn is its tumor-like structures that form on the aerial parts of the plant. Plants having these features are characterized as having smut disease.

Ustilago maydis is used often for its homeopathic remedies for the female genitalia. Common uses are for irritation of the ovaries, dark periods, non-menstrual bleeding (passive, non-passive, string bleeding), and pain in the ovaries or the womb, which includes cramping (ABC 2001-04). Some strains of the fungal pathogen emit killer toxins, such as KP6, which are further encoded by double-stranded RNA viruses in its cell cytoplasm (Li, 1999). It also is an excellent model used in analyzing phytopathogenesis in the molecular laboratory.

Interestingly, corn smut is a delicacy in Mexico. The elegant dish is called huitlacoche and it is created before the teliospores are ripe and the inside is moist. The gall must also be white to gray on the outside. Farmers appreciate this fungus because they can receive a high price relative to unaffected corn crop. Some farmers will introduce this fungus to their crops on purpose (Volk, 1998).

Genome structure

The current genome size of Ustilago maydis is approximately 20 million base pairs. Presently strain 521 has been sequenced. It is composed of a very highly conserved repetitive sequence. The Broad Institute in Cambridge, Massachusetts recently declared the genome at 19, 7 Mb. The genome includes 6,902 expected protein-encoding genes and does not have pathogenicity signatures in the sequence of hostile pathogenic fungi (Kamper, 2006).

Cell structure and metabolism

The composition of the cell wall is not completely deciphered. Recent studies indicate that the walls are made of mostly of polysaccharides and chitin. Chitin and phosphate are more abundant in the mycelial form that in the yeast (Ruiz-Herrara, 1998). Knowledge of the cell wall composition and metabolism of Ustilago maydis is still being investigated. However, recent studies have shown that cell walls of the yeast and mycelial forms are mostly made up of polysaccharides. Mycelial forms contain both polysaccharides and chitin (Feldbrugge, 2004).

Ustilago maydis is useful in studying many things, such as mating determination, homologous recombination and signaling pathways. This is because during the life cycle of U. maydis, non-pathogenic haploid cells, which grow like yeast, fuse together to form a dikaryotic hyphae (Bolker, ). U. maydis can only induce disease in the dikaryotic stage that occurs after mating. This process involves cAMP and mitogen-activated protein kinase (MAPK) signaling that regulate transcriptional and other morphological responses. One of the products made from the dikaryotic stage is a major regulator needed for pathogenic development. The major regulator then orchestrates a complex transcriptional cascade which has been uncovered by genomic strategies (Smith, 2003).

Signal transduction pathways are important for many of features of fungal metabolism. For example, many human fungal pathogens show some type of dimorphism, and a common element in these and other fungi is MAPK. Each pathway is made of a signal cascade involving the phosphorylation of three protein kinases. These kinases include a MAPK kinase kinase (MAPKKK), a MAPK kinase (MAPKK), and the MAPK. This protein, in turn, phosphorylates one or more target transcription factors and other substrates (Smith, 2003).

U. maydis is a pathogen of maize, for which cell fusion and pathogen development are controlled by two separate mating loci: a and b. The a locus encodes the pheromone and a seven-transmembrane protein pheromone receptor which constitute the cell recognition system. The b loci is required for control of pathogenic development. The pheromone-responsive MAPK pathway is involved in the activation of both the a and b loci (Smith, 2003).


Ustilago maydis is called smut due to the way galls appear on the corn due to dark teliospores. The teliospores allow the fungus to survive winter and drought conditions (Volk, 1998). Corn smut prefers dry conditions with the temperature being between 78°F to 93° F and occurs in greater quantity in soil with high nitrogen or manure content.


Ustilago maydis is often correlated with viral infections. The killer system can be divided into three groups; the killer strains constantly produce toxins that can be lethal to more sensitive strains. So any neutral strains or those that don't produce toxins, can be affected by the toxins of the killer strains. It is important to mention that the killer strains are immune to their own toxins but not those from strains around them (Moore-Landecker, 1996).

Ustilago maydis rely on plants to complete their life cycles. This parasitic fungus switches from the non-pathogenic haploid form to a pathogenic filamentous form due to the mating of haploid cells. This can only occur on the fungus’s corn host (Host-Parasite). In either form it is viewed as a pathogen of seeds and flowers of cereals, wheat, corn, and grasses. It is most common to invade corn crops and cause smut disease.

The teliospores fall off of the corn and spread via wind and in the spring they germinate to form basidia (UC Pest, 1996). The basidia make basidiospores which actually infect the corn and the fungus usually infects the kernels although it can spread to the tassels and stem. The infection decreases the ability of the corn to grow as it could impede pollination and the transport of materials and growth. As the fungus grows hypertrophy and hyperplasia occurs causing large tumors on the corn. Some corn is more resistant to the smut although no variety is completely resistant(Volk, 1998).

Current Research

Currently at Saint Joseph's University in Philadelphia, PA, field studies have shown that pollination can help protect corn ears from smut infection. A continuing project carried out by Dr. Michael McCann, with the collaboration of fellow students, has resulted in the isolation of Ustilago maydis mutants with defects that in actuality prevent them from infecting plants. They are currently using genetic, molecular, and other microscopic methods to study these mutants so we can further learn into the development of this fungus and its affect on plants (Snetselaar, 2003).


ABC Homeopathy. (2001-04). Ustilago maydis. Influenca ltd. Retrieved November 3, 2006 from [[1]]

Bölker, Michael. Ustilago maydis – a valuable model system for the study of fungal dimorphism and virulence. Universität Marburg, Fachbereich Biologie, Karl-von-Frisch-Strasse 8, D-35032 Marburg, Germany. (1999-2001). Factsheets on Chemical Biological and Warfare Agents. Retrieved November 3, 2006 from [[2]]

“Corn Smut”. Retrieved 10 November 2006 from [3]

Feldbrugge, M. Kamper J, , Steinberg G, Kahmann R. (2004). Regulation of mating and pathogenic development in Ustilago maydis. Dec;7(6):666-72 Max Planck Institute for Terrestrial Microbiology, Department of Organismic Interactions, D-35043 Marburg, Germany.

“Host-Parasite Interactions.” (2001). Fungal Genetics Conference. Retrieved November 10, 2006 from[[4]]

Kamper, J. (2006). Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis. Nature. November 2, 2002. Pages 97-101.

Li, N. (1999). Structure of Ustilago maydis killer toxin KP6 alpha-subunit. A multimeric assembly with a central core. The Journal of Biological Chemistry Vol 274(29). Pages 20425-31.

Madera, M., Vogel, C., Kummerfeld, S.K., Chothia, C. and Gough, J. (2004) "The SUPERFAMILY database in 2004: additions and improvements." Nucl. Acids Res., 32, D235-D239.

Moore-Landecker, E. (1996). Fundamentals of the Fungi. Ed. 4: 172, 407, 425. New Jersey: Prentice Hall.

Ruiz-Herrera, J. (1998). “The fungus Ustilago maydis from the Aztec cuisine to the research laboratory.” Internatl Microbiol. Mexico: Springer-Verlag Iberica.

Smith, David G. Maria D. Garcia-Pedrajas, Wei Hong, Zhanyang Yu, Scott E. Gold, and Michael H. Perlin. An ste20 Homologue in Ustilago maydis Plays a Role in Mating and Pathogenicity. Department of Biology, University of Louisville, Louisville, Kentucky, Department of Plant Pathology, University of Georgia, Athens, Georgia. Received 13 May 2003/ Accepted 3 December 2003

Snetselaar, Dr. K. (2003). Department of Biology at St. Joseph's University in Philladelphia, PA.

Volk, T.J. (1998). Smuts on the Internet. [[5]]

University of UC Davis. (2006). UC Pest Management Guidelines. Retrieved November 10, 2006 from [[6]]

Edited by Christine DeSanno, Sara Lizzo, Daniel Paoletti, & Joseph Salzillo, students of Dr. Kirk Bartholomew