Grants and Contracts Details
Description
Among the most destructive plant diseases are the so-called "rots", caused by necrotrophic fungi
that inflict substantial tissue damage on their hosts in advance of hyphal colonization. Although
they are sometimes considered unsophisticated in comparison to the more elegant biotrophs,
necrotrophic pathogenic fungi must also be highly specialized in order to successfully avoid, or
suppress, host resistance responses. The molecular basis for pathogenicity in most necrotrophic
fungi is unknown. This group contains many important plant-pathogenic fungal genera, including
Botrytis, Sclerotinia, Mycosphaerella, Fusarium, Leptosphaeria, and Colletotrichum. A significant
number of the organisms within this group are actually hemibiotrophs, causing relatively little
damage to susceptible hosts during the initial stages of colonization, and switching to a highly
damaging, necrotrophic mode of growth only after they have become established within host
tissues. Hemibiotrophic organisms offer a unique opportunity to compare and contrast
necrotrophic and biotrophic lifestyles within a single experimental system. This proposal is based
on the idea that valuable new information will be learned about molecular mechanisms of
virulence in necrotrophic fungi by characterizing the genetics of necrotrophy versus biotrophy, and
of the transition between these two phases, in the model hemibiotrophic organism Colletotrichum
graminicola. A mutant of this fungus has been produced that is specifically deficient in the ability to
make the transition from biotrophy to necrotrophy. A gene has been cloned, named CPR1, that is
responsible for this mutation. The predicted protein sequence of CPR1 is very similar to a
component of the eukaryotic microsomal signal peptidase complex. The goal is to understand the
role of this gene in the biotrophy-necrotrophy transition, as well as to begin to use the CPR1-
mutant as a genetic tool to identify other genes that are associated with necrotrophy versus
biotrophy. The objectives of the research proposed here are to test the following three
hypotheses that are related to these goals: 1) CPR 1 does encode a component of a signal
peptidase; 2) Expression of CPR1 is up-regulated during necrotrophic growth; and 3) Differences
exist in fungal gene expression during necrotrophy versus biotrophy.
Status | Finished |
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Effective start/end date | 9/15/02 → 3/14/06 |
Funding
- Cooperative State Research Education and Extension: $195,000.00
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