Fungal genome exposes a "corny" plot
An ear of corn infected with Ustilago maydis
Photo courtesy of Dr. Christine D. Smart, Cornell University
Ustilago maydis may not be a household name, but it is well known among plant specialists. Nicknamed "corn smut," the fungus preys on corn to hinder plant growth and diminish harvests, often delivering a sizeable blow to economies that depend on the crop. Now, the efforts of an international research team to decode and analyze the U. maydis genome cast new light on the machinery that enables the fungus to do its dirty work. The paper describing this work appears in the November 2 issue of Nature.
As its nickname implies, U. maydis is one of a family of parasites called smuts (also known as "biotrophs"), which depend on living — not dead — tissue to grow and thrive. As such, biotrophs employ less aggressive tactics than other pathogenic fungi because they must live off of, but not kill, their hosts to ensure their own survival. The genetic factors that govern this silent invasion — in U. maydis or other biotrophs — are not known.
To gain insights into how biotrophy is regulated at the DNA level, a scientific team including researchers at BayerCropScience AG, the Broad Institute and Exelexis worked to sequence and analyze the U. maydis genome. This sequencing effort, which involves scientists from over 20 additional research centers, is part of the Broad Institute's Fungal Genome Initiative, a collaboration with the fungal research community to select fungal candidates for genome sequencing based on their roles in biomedicine, agriculture, and industry, as well as their importance to comparative genomic projects.
One of the most striking findings involves secreted proteins — that is, proteins released to the outside world. Unlike other pathogenic fungi, U. maydis possesses relatively few secreted proteins to destroy the tough outer shells of plant cells, a result that might otherwise been predicted given its biotrophic habits. But, to the scientists' surprise, the fungus contains a large number of other secreted proteins, the functions of which are largely unknown. Curiously, the genes encoding these obscure proteins are arranged in several different clusters, which are scattered throughout the U. maydis genome and are highly active during infection.
To explore the importance of these gene clusters to fungal infection, the scientists systematically removed each one from the U. maydis genome. For some clusters, this crippled the fungus' growth, suggesting the genes are involved in driving infection. Interestingly, the removal of one particular cluster actually boosted the fungus' invasive abilities, implying that its genes normally act as restraining influences. Together, these findings provide the first inroads to delineate the factors that underlie the virulence of U. maydis as well as other biotrophic fungi.
The project was led by Bruce Birren, head of the Broad's Fungal Genome Initiative, and included the Broad's Genome Sequencing Platform as well as Genome Biology Program scientists Jonathan Butler, Sarah Calvo, Dave DeCaprio, James Galagan, David Jaffe, Li-Jun Ma, Evan Mauceli, Chad Nusbaum, Claire Wade, and Sarah Young.
Kämper, J et al. (2006) Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis. Nature; doi:10.1038/nature05248