Showing papers on "Mycovirus published in 1996"
TL;DR: Progress is focused on progress in elucidating mechanisms by which hypoviruses alter fungal gene expression and the insights that these surprising results present for further understanding of signal transduction processes that underlie fungus-plant pathogenic interactions.
Abstract: Imagine the task of designing a reagent to explore regulatory mechanisms that govern fungal pathogenesis. The assignment triggers recollection of a group of cytoplasmically transmissible RNA mycoviruses that have the property of attenuating fungal virulence. Utility of these viruses is significantly enhanced by the construction of an infectious cloned cDNA copy of the viral RNA genome. Subsequent studies reveal that virus infection attenuates fungal virulence by altering cellular signal transduction processes, thus exposing a role for G protein-linked, cAMP-mediated signaling in fungal pathogenesis. Synthetic transcripts derived from the infectious viral cDNA are used to establish virus infection in pathogenic fungi other than the natural host, thereby expanding opportunities for probing and manipulating a broader range of plant-pathogen interactions. As a bonus, the infectious viral cDNA is found to provide enhanced potential for biological control of fungal disease. Elements of the account presented above represent actual developments derived from recent molecular analyses of mycoviruses, taxonomically grouped within the genus Hypovirus of the family Hypoviridae, that attenuate virulence of the chestnut blight fungus Cryphonecrria parasitica. Details of the intriguing biology and potential applications offered by this system have been the subject of several recent reviews (MacDonald and Fulbright, 1991; Nuss, 1992; Heiniger and Rigling, 1994). This article discusses recent progress on two major fronts. The first involves advances in the development of hypovirus molecular biology and the extended experimental and practical utility provided by these advances. The second focuses on progress in elucidating mechanisms by which hypoviruses alter fungal gene expressionNirulence and the insights that these surprising results present for further understanding of signal transduction processes that underlie fungus-plant pathogenic interactions.
86 citations
TL;DR: It is hypothesized that the four genes are coordinately down-regulated by the virus and probably are associated in a regulatory cascade, and this hypothesis was tested by measuring the relative transcription rate of each gene in virus-infected and uninfected isogenic strains of the fungus by using nuclear run-on assays.
Abstract: The hypovirus CHV1, which infects the plant-pathogenic fungus Cryphonectria parasitica, causes a distinct range of symptoms in its host that include reduced virulence expression, reduced sporulation, and reduced pigmentation. The virus, however, has little or no effect on fungal growth in culture. The visual symptoms are associated with reduced accumulation of a small number of host mRNAs and proteins. Four of the host genes encoding these down-regulated mRNAs have been characterized; they include two genes encoding a fungal sex pheromone (Vir1 and Vir2), a gene encoding an extracellular laccase (Lac1), and a gene encoding a cell wall hydrophobin (Crp). Expression of most other host proteins appears to be unaffected by the virus. These four genes can serve as reporter genes in studies of the effect of the virus on host gene expression. It is hypothesized that the four genes are coordinately down-regulated by the virus and probably are associated in a regulatory cascade. This hypothesis was tested by measuring the relative transcription rate of each gene in virus-infected and uninfected isogenic strains of the fungus by using nuclear run-on assays. The effects of the virus on transcription of these genes generally mirrored the observed effects of the virus on relative accumulation of the mRNAs of each gene. Although repressed transcription cannot account for all of the effects of the virus on mRNA accumulation of these four reporter genes, it is the predominant effect.
72 citations
TL;DR: A mycovirus from the phytopathogenic fungus, Fusarium solani f.
Abstract: A mycovirus (named FusoV) from the phytopathogenic fungus, Fusarium solani f. sp. robiniae SUF704, has two kinds of double-stranded (ds) RNA genomes, designated M1 and M2. The cDNAs were constructed from FusoV genomic dsRNAs. The sequences of M1 and M2 cDNAs comprised 1645 and 1445bp, respectively. Sequence analysis showed that each dsRNA had a single long open reading frame (ORF) on only one of the strands. M1 ORF encodes a 519-amino acid residue polypeptide with a predicted molecular mass of 60 kDa. RNA-dependent RNA polymerase-conserved motifs were identified in the predicted amino acid sequence, and the polymerase synthesized dsRNA in vitro. The M2 ORF encodes a polypeptide of 413 amino acid residues with a predicted molecular mass of 44 kDa. The predicted amino acid sequence contained the sequence corresponding to those found in the purified 44-kDa capsid protein of FusoV.
55 citations
01 Jan 1996
TL;DR: Hypovirulence may be transmissible, involving dsRNA mycoviruses as in the case of Cryphonectria parasitica, or non transmissible as in Rhizoctonia spp.
Abstract: Expression of virulence by populations of any pathogen is generally a continuum between two extremes; high virulence and avirulence. Low virulent to avirulent isolates are considered hypovirulent. At some point along this continuum however, hypovirulence ends and virulence begins (Van Alfen, 1982). Hypovirulence may be transmissible, involving dsRNA mycoviruses as in the case of Cryphonectria parasitica (Van Alfen, 1982), or non transmissible as in Rhizoctonia spp. (Ichielevich-Auster et al., 1985a; Finkler et al., 1985).
36 citations
TL;DR: Results suggest that FusoV genomic dsRNA replicates in a conservative manner, and are likely to be of positive polarity for both M1 and M2 by dot blot hybridization analysis.
Abstract: A mycovirus (named FusoV) from the plant pathogenic fungus Fusarium solani possessed two types of double-stranded (ds) RNA genome, designated Ml and M2. RNA-dependent RNA polymerase activity was detected in FusoV particle fractions. An in vitro RNA polymerase reaction using purified FusoV particles that was supplemented with NTPs revealed the synthesis of single-stranded (ss) RNA species and a subsequent formation of dsRNAs having the same size as Ml and M2. The ssRNA species synthesized in the first stage were proved to be of positive polarity (coding strand) for both M1 and M2 by dot blot hybridization analysis. These results suggest that FusoV genomic dsRNA replicates in a conservative manner.
6 citations
01 Jan 1996
TL;DR: A model in which Zb-M killer viruses lead to a suicidal phenotype of haploid segregants under conditions in which Kex3p is fully expressed and an additional mutation within either of two chromosomally encoded toxin-sensitivity genes (TOS1 and/or TOS2) is present is described.
Abstract: The killer toxin-secreting yeast Zygosaccharomyces bailii 412 contains two cytoplasmically inherited double-stranded RNA (dsRNA) viruses (ZbV-L, ZbV-M) responsible for the expression of a killer phenotype in its infected host. While ZbV-L functions as a classical helpervirus by providing capsid (cap) and RNA polymerase functions (cap/pol) necessary for packaging and replication of both viruses, M-dsRNA-containing killer viruses (ZbV-M) are satellites of ZbV-L that contain the genetic information for toxin production only. Both viruses were shown to be sufficient to confer the Z. bailii killer phenotype upon transfected spheroplasts of a S. cerevisiae non-killer strain, resulting in toxin-secreting transfectants. Genetic analysis of transfected S. cerevisiae strains indicated that the heterologous expression of a Z. bailii killer phenotype depends on the expression of a single chromosomal gene: KEX3. Thus, kex3 mutants of S. cerevisiae are phenotypically non-killers showing normal, i.e. wild-type levels of the toxin-coding M-dsRNA. In the genetic background of a kex3 mutation, the stably maintained ZbV-M killer viruses would be regarded as “cryptic”, because of the lack of any dsRNA-associated phenotype. Cytoductive transfer of ZbV-M from “cryptic” non-killers into KEX3 non-killer recipient strains resulted in heterozygous (kex3/KEX3) diploids that expressed a strong killer phenotype. However, meiotic segregants derived from dissection of kex3/KEX3 diploids showed (a) a loss in cell viability and (b) a significant selection of a certain genotype among the surviving haploid progenies. We describe a model in which Zb-M killer viruses lead to a suicidal phenotype of haploid segregants under conditions in which Kex3p is fully expressed and an additional mutation within either of two chromosomally encoded toxin-sensitivity genes (TOS1 and/or TOS2) is present. Survival of these strains is only possible in the presence of a kex3 mutation, leading to stably maintained ZbV-M viruses that, because of the lack of any detectable phenotype, would be regarded as “cryptic”. In this respect we discuss a more general model postulating a remarkable effect of such “cryptic” mycoviruses on the evolution of the virus-infected host.
3 citations