research: Fungal molecular biology and genetics

 

Understanding an organism’s response to external stimuli as it relates to host-pathogen interactions is essential to gaining insight into the pathogenesis of disease. The fungus that we work with, Cryphonectria parasitica, serves as an excellent model system for studying such interactions both at the plant-fungal interface as well as the virus-host level. This plant pathogen is responsible for chestnut blight, a disease that resulted in the loss of approximately 4 billion American chestnut trees in the early 20th century.

We are very fortunate to be funded by the National Science Foundation:

MCB-0718735 (2007 - 2011)

MCB-1051453 (2011 - 2015)

In the laboratory C. parasitica can be easily cultured and manipulated, which allows us to ask basic but directed questions about its behavior and development. C. parasitica can itself be infected by an RNA virus and a virus-infected strain exhibits a number of changes from an uninfected one, the most striking of which is a reduction in the ability to cause significant damage to chestnut. Because of the reduction in fungal virulence, we call this virus a “hypovirus”.

Since we can genetically modify both the hypovirus and the fungus, we have a powerful system that permits us to explore the interactions of an RNA virus and its eukayotic host. Also, the hypovirus provides a tool to investigate molecular mechanisms of plant pathogenesis as well as other behavior and developmental pathways in C. parasitica.

Research in my laboratory covers techniques in molecular biology, biochemistry, genetics and “omics” (genomics, transcriptomics and metabolomics). We are in the process of identifying genes important in various signaling pathways in the fungus that control how this organism responds to external stimuli - an essential ability for pathogenesis but also a feature compromised by virus infection. We identify genes of interest via comparative genomic and classical genetic methods and test hypotheses about the functions of the proteins they make.

Current and recent projects include:


  1. 1.Understanding the pathways that control anastomosis (the ability of two fungal colonies to fuse, a process important for virus transfer), and the identification of stimuli that trigger an incompatible response (see the recent paper in Genetics).

  2. 2.Developing structural models for untranslated regions of the viral genome using RNase digestion and computation modeling (see paper in Virus Research, 2011).

  3. 3.Investigating other physiological responses to virus infection including response to light, alterations that the virus causes to central metabolic pathways (published in 2009 in Microbiology) and developing new molecular tools for the organism, such as an inducible promoter system (published in 2009 in Applied and Environmental Microbiology).

  4. 4.Analyzing the post-translational modifications of a phosducin-like protein called BDM-1 that is required for G-protein signaling (see 2010 paper in Molecular Microbiology).


See the publications page for all the latest developments.


Canker size produced by wild type and hypovirulent C. parasitica. From Dawe and Nuss, Ann. Rev. Genet, 2001.

 

A C. parasitica colony of strain EP155 at approximately one week.

 

Link to the Cryphonectria genome project

 

Gene knock-outs that affect pigmentation and sporulation. See Salamon et al., 2010.

 

Controlled expression of a reporter protein under different culture conditions. See Willyerd et al., 2009.