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Dr.
Scott Kroken
Division of Plant Pathology and Microbiology
Assistant Professor
Marley Building, Room 341C
Phone: 520-626-7972
Email: kroken@ag.arizona.edu
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Visit
these web-sites to learn more about Dr. Kroken and his research
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| Background
and Interests |
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recent evolutionary studies look for the pattern of evolution through
phylogenetic and population genetic studies, using selectively neutral
molecular markers. The results of these studies have been used to
infer the processes of evolution, such as adaptation and diversification.
As we come to understand which genes direct which processes in an
organism, we can begin to study how these genes adapt an organism
to its environment, and how these functions vary among different
lineages. The goal of my research program is to investigate fungal
species for these types of genetic changes that can result in key
phenotypic changes. My approaches include: 1) determining the origins
and population dynamics of virulent lineages of fungal pathogens
in agriculture and medicine, 2) characterizing the evolution and
inheritance of secondary metabolite genes and gene clusters, and
the roles of their products in pathogen-host interactions, and 3)
the use of comparative genomics and proteomics to identify differences
among closely related fungi, and commonalities among distantly related
fungi. |
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| Projects |
Evolution
of secondary metabolism in euascomycete fungi
Up to 5% of the genomes of euascomycete fungi are occupied by gene
clusters that encode biochemical pathways for a diversity of polyketides,
nonribosomal peptides, alkaloids, terpenoids, and combinations of
these building blocks, to produce an array of mycotoxins that poison
animals (e.g cyclosporin, lovastatin, fumonisin), phytotoxins that
act as pathogenicty factors on plants (e.g T-toxin, AAL-toxin, HC-toxin),
and antibacterials that deter their bacterial competitors (e.g. penicillin).
Genomic comparisons show that all euascomycete fungi, regardless of
nutritional mode (plant or animal pathogen, endophyte, or saprobe)
share the same classes of secondary metabolite genes. Therefore, this
genetic legacy has been used by diverging lineages of fungi for diverse
biotic interactions as they evolved to occupy new niches. Among the
questions I am trying to answer are: how does the expansion of gene
families occur? What are the relative roles of gene loss cf. horizontal
gene transfer? How do novel metabolic pathways form? Why do the constituent
genes of each pathway occur in gene clusters, whereas other functionally
related genes are scattered throughout the genome of a eukaryotic
organism?
Co-evolution of fungal pathogens
with teosinte to maize
Agricultural epidemics occur when novel strains of fungi appear
that are virulent on monocultures of plants. We usually have no
idea of how these strains arise or where they come from. Hypotheses
of mutation, recombination, or horizontal gene transfer of a virulence
factor are proposed to explain the former question. The latter question
is usually addressed by invoking host jumps from surrounding plants
(e.g. weeds) that may be closely or distantly related, or by long-distance
dispersal from distant populations. As a model system, I plan to
investigate the fungi that occur on wild population of teosinte
in Mexico, where this progenitor of maize is endemic, and compare
these fungi to those that are found on descendent cultivated populations
of maize. Two speices of Fusarium that are significant pathogens
of maize have already been found on teosinte. These and other fungi
may serve as models for the co-evolution of fungus and host, in
terms of pathogenicity and virulence factors, which may include
secondary metabolites, and in terms of their population genetics,
which may feature broader genetic diversity in the fungi in wild
populations cf. agricultural populations and thus exist as reservoirs
for novel virulent strains.
Evolution of pathogenicity
factors and conditionally dispensable chromosomes in the plant pathogen
Nectria haematococca
This pathogen of pea contains an enzyme (pisatin demethylase) that
detoxifies the phytoalexin (pisatin), which is produced to deter
fungal infections. Only strains of this fungus that have this ability
can colonize pea and cause significant disease. This gene resides
on a small chromosome that can be lost, with the only evident phenotypic
change being the loss of the ability to be a pathogen of pea. We
are investigating the origin of pisatin demethylase, which is a
P450 cytochrome, and thus a member of a huge gene superfamily. A
gene genealogical approach will indicate when this P450 diverged
and evolved the ability to detoxify pisatin, and whether the known
orthologs of this gene found in polyphyletic pathogens of pea were
inherited vertically from a common ancestor, or gained by horizontal
gene transfer in a common infection court. We are also investigating
the structure and inferring the origin of the conditionally dispensable
chromosome, which is part of the larger project to sequence the
genome of this fungus. This project is a collaboration with Hans
Van Etten.
Population genetics of Coccidioides
posadasii, cause of Valley Fever in Arizona
Valley Fever is the most common nonsexally transmitted disease in
Arizona. We are investigating the fungus that causes this disease,
in order to determine if this species is structured by geography
(is gene flow limited within Arizona?) by site (is clonality important?
do rodents play a role in the patchy distribution of Coccidioides
in soil?), by host (are humans, dogs, rodents and other species
all susceptible to the same strains?). This information will be
useful to understanding the epidemiology and pathology of this disease,
and may help design strategies to reduce the incidence of this disease.
This project is a collaboration with John Galgiani (VA) and Marc
Orbach. This product will be the basis of graduate student Bridget
Barker’s Ph.D. dissertation.
Comparative proteomics of
euascomcyete fungi in response to their symbiotic hosts (Bio5 initiative)
We are looking for secreted factors in common to euascomycete fungi
that interact with a range of host organisms, in order to understand
how these fungi evolved so many different trophic interactions from
an ancestral genome. The ultimate goal is making use of these common
features as targets against pathogenic fungi.
The fungus/host systems we are using include:
The animal pathogen Coccidioides posadasii on mouse (John Galgiani)
The opportunistic animal pathgen Aspergillus flavus on mouse (Peter
Cotty)
The animal allergen Alternaria sp. on mouse (Barry Pryor)
The plant pathogen Magnaporthe grisea on rice (Marc Orbach)
The plant pathogen Nectria haematococca MPVI on pea (Hans Van
Etten)
The endophyte Xylaria sp. on poplar (Betsy Arnold)
The lichenized fungus Cladonia grayi with unicellular green algae
(Scott Kroken)
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| Publications |
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Mandel MA Galgiani JN Kroken S Orbach MJ. Nov 2006. Coccidioides posadasii contains single chitin synthase genes corresponding to classes I to VII. Fungal Genet Biol, 43:775-88
Baker SE, Kroken S, Inderbitzin P, Asvarak T, Li BY, Shi L, Yoder OC, Turgeon BG. Feb 2006. Two polyketide synthase-encoding genes are required for biosynthesis of the polyketide virulence factor, T-toxin, by Cochliobolus heterostrophus. Mol Plant Microbe Interact, 19:139-49
Lee BN, Kroken S, Chou DY, Robbertse B, Yoder OC, Turgeon BG. Mar 2005. Functional analysis of all nonribosomal peptide synthetases in Cochliobolus heterostrophus reveals a factor, NPS6, involved in virulence and resistance to oxidative stress. Eukaryot Cell, 4:545-55
Kroken S, Glass NL, Taylor JW, Yoder OC, Turgeon BG. Dec 2003. Phylogenomic analysis of type I polyketide synthase genes in pathogenic and saprobic ascomycetes.. Proc Natl Acad Sci U S A, 100(26):15670-15675
Lu SW, Kroken S, Lee BN, Robbertse B, Churchill AC, Yoder OC, Turgeon BG. May 2003. A novel class of gene controlling virulence in plant pathogenic ascomycete fungi.. Proc Natl Acad Sci U S A, 100(10):5980-5985
Galagan JE et al. Apr 2003. The genome sequence of the filamentous fungus Neurospora crassa.. Nature, 422(6934):859-868
Paszkowski U, Kroken S, Roux C, Briggs SP. Oct 2002. Rice phosphate transporters include an evolutionarily divergent gene specifically activated in arbuscular mycorrhizal symbiosis.. Proc Natl Acad Sci U S A, 99(20):13324-13329
Hogberg N, Kroken S, Thor G, Taylor JW. Jul 2002. Reproductive mode and genetic variation suggest a North American origin of European Letharia vulpina.. Mol Ecol, 11(7):1191-1196
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