A postdoctoral position is available starting in Sept. 1995 with funding
for at least two years. The location is Athens, Georgia a great town!.
The University of Georgia is an excellent place to study mycology. Below
is a summary of the project. For more info please contact me at
sgold at uga.cc.uga.edu.
The Genetics of Fungal Dimorphism and Pathogenicity in Ustilago maydis.
This project addresses the long-term goal of understanding the genetic
control of morphogenesis and pathogenicity in fungi. We will approach this
goal by elucidating the underlying mechanisms controlling yeast-hypha
transitions in Ustilago maydis, the causal agent of corn smut disease.
This is important because many fungi, including saprophytes and pathogens
of animals and plants, alternate between filamentous and budding growth
morphologies (fungal dimorphism) in response to environmental and genetic
conditions. Additionally, growth phase is often correlated with virulence.
In wild U. maydis only the filamentous stage is pathogenic. The
filamentous form is generated in the dikaryon formed upon the mating of two
compatible budding haploids.
Our recent discovery that the cAMP pathway plays a significant role in
dimorphism of U. maydis has made a further dissection of morphogenesis
possible (Gold et. al, Genes and Development 1994). Specifically, we have
isolated the U. maydis adenylate cyclase gene (uac1) which is required for
budding growth. Upon disruption of the uac1 gene, filamentous strains are
generated from previously normal budding haploids. Additionally, we have
collected 45 mutants which are suppressed for the filamentous phenotype of
adenylate cyclase mutants. These strains are termed ubc for Ustilago
bypass of cyclase and display budding growth. Complementation of one of
these ubc supressor mutations led to the isolation of the gene (ubc1)
encoding the regulatory subunit of cAMP dependent protein kinase (rPKA)
which is required for normal post mating filamentous growth and
responsiveness to environmental signals. Preliminary data also indicate a
role for the ubc1 gene in normal corn smut disease progression. Further
characterization of genes of this pathway will yield a better understanding
of the genetic control of dimorphism and pathogenicity in U. maydis and
other dimorphic fungi. These studies may uncover the target genes of the b
mating type locus which encodes homeodomain proteins controlling the
post-mating shift to filamentous growth. It may also be possible to
identify new fungal targets for disease control strategies based on a
better understanding of the genes involved in pathogenicity.
The specific aims of this proposal are to:
A) define complementation groups of, and clone the genes responsible for,
the ubc class of suppressor mutations: This work will provide insight into
the genetic basis of filamentous growth. The primary questions asked here
are; how many different genes are involved in bud-hypha transitions, what
are their functions, and how do they relate to each other to create a
morphogenetic pathway? This is important for the pathogenicity of the smut
fungi and of general relevance to mycology as filamentous growth is a
hallmark of the absorptive feeding habit of the kingdom mycota;
B) further characterize the interaction between ubc1 mutants and the host
plant: This work will further characterize the defect in the pathogenicity
of ubc1-1 (rPKA) mutants and should shed light on the normal infection
process. The primary question asked here is; what stage in the infection
process is affected in the ubc1-1 mutant? This work will establish the
basis for studies of the relationship between genes controlling dimorphism
and the intricate interactions between fungus and plant leading to the
production of large galls and to teliosporogenesis.