Deng Fuyou, Allen Todd D, Hillman Bradley I, Nuss Donald L
Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, 9600 Gudelsky Drive, Rockville, MD 20850, USA.
Eukaryot Cell. 2007 Aug;6(8):1286-98. doi: 10.1128/EC.00166-07. Epub 2007 Jun 8.
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.
栗疫病菌(Cryphonectria parasitica)被低毒病毒CHV1-EP713、呼肠孤病毒MyRV1-Cp9B21或MyRV2-CpC18感染后,其毒力会降低(产生低毒性)。然而,这两组真菌病毒引起的其他表型变化却大不相同。我们现在报告,低毒病毒感染后观察到的雌性交配能力丧失以及由此导致的通过有性孢子传播病毒的缺失,在呼肠孤病毒感染的寄生隐孢壳菌中并未观察到。与这一结果一致的是,参与有性生殖的两个基因,即信息素前体基因Mf2/1和酵母STE12样转录因子基因cpst12,在呼肠孤病毒感染的菌株中的表达量降低程度低于低毒病毒CHV1-EP713感染的菌株。使用定制的微阵列cDNA芯片进行分析,该芯片包含代表约2200个独特寄生隐孢壳菌基因的表达序列标签克隆,分别鉴定出140个和128个对MyRV1-Cp9B21或MyRV2-CpC18感染有反应的宿主基因。对这些病毒反应基因的比较显示,尽管两种呼肠孤病毒的核苷酸序列同一性低于50%,但仍有85个基因重叠。值得注意的是,85个基因中的84个在相同方向上发生了改变。进一步比较发现,MyRV1-Cp9B21和MyRV2-CpC18反应基因中分别有51%和48%也对CHV1-EP713感染有反应。最后,与报道的CHV1-EP713感染结果相似,在细胞G蛋白信号转导途径被破坏后,高比例(59%和66%)的呼肠孤病毒反应基因也发生了差异表达。这些数据支持了这样一种假设,即低毒病毒和呼肠孤病毒感染会扰乱寄生隐孢壳菌共同的和特定的调控途径,从而导致低毒性和不同的表型变化。