Mechanism of the Transition Between Biotrophy and Necrotrophy in a Hemibiotroph

Grants and Contracts Details


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.
Effective start/end date9/15/023/14/06


  • Cooperative State Research Education and Extension: $195,000.00


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