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Eukaryotic Cell, August 2007, p. 1286-1298, Vol. 6, No. 8
1535-9778/07/$08.00+0     doi:10.1128/EC.00166-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Comparative Analysis of Alterations in Host Phenotype and Transcript Accumulation following Hypovirus and Mycoreovirus Infections of the Chestnut Blight Fungus Cryphonectria parasitica{triangledown}

Fuyou Deng,1 Todd D. Allen,1,{dagger} Bradley I. Hillman,2 and Donald L. Nuss1*

Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, 9600 Gudelsky Drive, Rockville, Maryland 20850,1 Department of Plant Biology and Pathology, Rutgers University, New Brunswick, New Jersey 08901-85202

Received 9 May 2007/ Accepted 24 May 2007

Infection of the chestnut blight fungus, Cryphonectria parasitica, by hypovirus CHV1-EP713 or by reovirus MyRV1-Cp9B21 or MyRV2-CpC18 results in reduced fungal virulence (hypovirulence). However, additional phenotypic changes caused by the two groups of mycoviruses are quite different. We now report that the loss of female fertility and the resulting absence of virus transmission through sexual spores observed after hypovirus infection was not observed for reovirus-infected C. parasitica. Consistent with this result, expression of two genes involved in sexual reproduction, the pheromone precursor gene, Mf2/1, and the yeast STE12-like transcriptional factor gene, cpst12, was less reduced in reovirus-infected strains than in the hypovirus CHV1-EP713-infected strain. Analysis with a custom microarray cDNA chip containing expressed sequence tag clones representing approximately 2,200 unique C. parasitica genes identified 140 and 128 host genes that were responsive to MyRV1-Cp9B21 or MyRV2-CpC18 infection, respectively. Comparison of these virus-responsive genes revealed an overlap of 85 genes, even though the nucleotide sequence identity for the two reoviruses is less than 50%. Significantly, 84 of the 85 genes were altered in the same direction. Further comparison revealed that 51% and 48% of the MyRV1-Cp9B21- and MyRV2-CpC18-responsive genes were also responsive to CHV1-EP713 infection. Finally, similar to results reported for CHV1-EP713 infection, a high percentage (59% and 66%) of the reovirus-responsive genes were also differentially expressed following disruption of the cellular G-protein signal transduction pathway. These data support the hypothesis that hypovirus and reovirus infections perturb common and specific C. parasitica regulatory pathways to cause hypovirulence and distinct sets of phenotypic changes.

* Corresponding author. Mailing address: Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, 9600 Gudelsky Drive, Rockville, MD 20850. Phone: (240) 314-6218. Fax: (240) 314-6255. E-mail: nuss{at}umbi.umd.edu

{triangledown} Published ahead of print on 8 June 2007.

{dagger} Present address: Harrisburg Area Community College—Lancaster, 206R, 1641 Old Philadelphia Pike, Lancaster, PA 17602.

Eukaryotic Cell, August 2007, p. 1286-1298, Vol. 6, No. 8
1535-9778/07/$08.00+0     doi:10.1128/EC.00166-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Guo, L.-h., Sun, L., Chiba, S., Araki, H., Suzuki, N. (2009). Coupled termination/reinitiation for translation of the downstream open reading frame B of the prototypic hypovirus CHV1-EP713. Nucleic Acids Res 37: 3645-3659 [Abstract] [Full Text]  
  • Sun, L., Suzuki, N. (2008). Intragenic rearrangements of a mycoreovirus induced by the multifunctional protein p29 encoded by the prototypic hypovirus CHV1-EP713. RNA 14: 2557-2571 [Abstract] [Full Text]  


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