West Lafayette, Indiana
March 24, 2008
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A gene in the
fungus Fusarium verticillioides plays a major
role in the pathogen invading corn and also in
production of a potentially deadly toxin,
according to research led by Purdue plant
pathologist Charles Woloshuk.
The toxin is one of a group called mycotoxins
that can make people and most domestic livestock
ill.
(Tom Campbell/Purdue Agricultural Communication
photo) |
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Discovery that a specific gene is
integral to both fungal invasion of corn and development of a
potentially deadly toxin in the kernels may lead to ways to
control the pathogen and the poison.
Purdue University researchers evaluated the fungal gene ZFR1 and
found that it is vital to the process of the fungus growing on
corn kernels. Production of the toxin decreased when the
scientists disabled the gene.
At certain levels, the toxin can cause illness in humans and
most domestic livestock. Horses and pigs are at particular risk
and can develop fatal diseases by ingesting feed containing one
of a group of toxins called fumonisins (few-mahn-ah-sins). About
$40 million of the U.S. corn crop is lost annually due to
presence of these toxins, according to experts.
"Our main research question has been what triggers toxin
production when the fungus attacks the corn kernel; it appears
that kernel starch plays an important role," said Charles
Woloshuk, a Purdue University
plant pathologist. "When ZFR1 is deleted, the resulting
mutant fungus has a problem transporting sugars that are
produced from the degradation of kernel starch."
The resulting sugars must be transported to cells as fuel for
other biochemical processes.
"The pathogen - the fungus Fusarium verticillioides - has a
number of putative sugar transporter genes that are expressed
during its growth on kernels and toxin production," Woloshuk
said. "Disruption of ZFR1 also affects expression of the sugar
transporter genes."
Woloshuk and his colleague, Bert Bluhm, now at the University of
Arkansas, report in the current issue of Molecular Plant
Pathology that when the gene ZFR1 is turned off, it reduces
manifestation of genes involved in production of the most
prevalent and dangerous fumonisin, FB1.
The researchers studied ZFR1 regulation of fungal growth and
toxin production in the starch-rich areas of corn kernels and
the conversion of starch to glucose, glucose recognition and the
expression of sugar transporter genes. From this information,
Woloshuk and his team identified a specific sugar transporter,
FST1 (fusarium sugar transporter1), that is necessary for FB1
production.
Although FST1 is required for FB1 production, it is not involved
with the fungus infecting corn kernels. This led the scientists
to hypothesize that FST1 acts as a molecular sensor necessary
for toxin production.
Kernels with lower starch content, most notably immature
kernels, don't support toxin production, Woloshuk said. This is
evidence that the kernel makeup dictates how this pathogen
controls toxin production.
Corn and fungal growth were unaffected when the sugar
transporter gene was disrupted, but toxin production on the
kernels was cut by about 82 percent, Woloshuk said.
When fusarium invades corn in the field, it causes an ear rot
disease. Even knowing that ear rot is present doesn't help
identify corn containing toxin because obvious signs of the
fungus don't correlate with presence of toxins. The only way to
confirm toxin is present is to test for it. Testing is so
expensive, however, that it usually isn't done unless the
disease is highly evident.
Weather and insect damage impact development of a variety of
fungi and toxins and also influence the level of poisons that
are present. Toxins are more likely to develop in corn when hot,
dry weather is followed by highly humid or wet weather.
The group of toxins associated with varieties of fusarium
species are known as mycotoxins. Some clinical evidence links
these toxins with certain human cancers.
Grains grown for cereal and feeds are susceptible to one or more
of the fusarium fungi species. Wheat and barley attacked by one
of the species closely related to Fusarium verticillioides can
develop head blight and accumulate mycotoxins, causing billions
of dollars in crop losses worldwide.
Further study is needed because the researchers still don't know
what triggers the biochemical process that regulates ZFR1 and
consequently leads to toxin production, Woloshuk said. The
scientists also are investigating the sugar transporter genes to
discover if they have other roles in the fungus and what
molecular interactions between the fungus and the plant allow
infection and toxin production.
"We're closer to finding some of the triggers in corn that
assist the fungus in toxin production," Woloshuk said.
The other researchers involved in this study were Department of
Botany and Plant Pathology doctoral student Hun Kim and Robert
Butchko of the USDA National Center for Agricultural Utilization
Research Service in Peoria, Ill. Bluhm is a former graduate
student in Woloshuk's laboratory who recently joined the
University of Arkansas faculty as an assistant professor.
A USDA-National Research Initiative grant provided support for
this work.
ABSTRACT
Involvement of ZFR1of Fusarium Verticillioides in Kernel
Colonization and the Regulation of FST1, a Putative Sugar
Transporter Gene Required for Fumonisin Biosynthesis on Maize
Kernels
Bert Bluhm, Hun Kim, Robert Butchko and Charles Woloshuk
Fumonisins comprise a class of carcinogenic mycotoxins produced
by Fusarium verticillioides during colonization of maize
kernels. In previous work, we identified ZFR1, which is
predicted to encode a Zn(II)2Cys6 zinc finger transcription
factor required for fumonisin B1 (FB1) production during growth
on kernels. In this study, we characterized the role of ZFR1 in
colonizing maize kernels and inducing FB1 biosynthesis. The ZFR1
deletion strain (Δzfr1) grew approximately 2.5-fold less than
the wild-type on endosperm tissue and a variety of other carbon
sources, including glucose and amylopectin. However, the
zfr1strain displayed higher amylase activity and expression of
genes involved in starch saccharification than the wild-type,
thus indicating that the reduced growth of the Δzfr1 strain was
not due to inhibition of amylolytic enzymes. In the wild-type
strain, expression of six genes encoding putative sugar
transporters was significantly greater on endosperm tissue than
on germ tissue, and expression of at least three of the six
genes was negatively affected by disruption of ZFR.
Intriguingly, disruption of FST1 had no effect on growth, kernel
colonization or kernel pH but decreased FB1 production by
approximately 82% on maize kernels. Based on these findings, we
hypothesize that ZFR1 controls FB1 biosynthesis by regulating
genes involved in the perception or uptake of carbohydrates. |
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