Cryphonectria parasitica
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA492223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR7881290.fastq.gz | Fastqsanger.gz | |||
| SRR7881300_1.fastq.gz | Fastqsanger.gz | |||
| SRR7881300_2.fastq.gz | Fastqsanger.gz | |||
| SRR7881310.fastq.gz | Fastqsanger.gz |
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Project description:Parasitic fungus that causes Chestnut Blight
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Project description:Here we report a comprehensive and comparative study comprising mitochondrion quantification, reactive oxygen species (ROS) and respiratory efficiency, and quantitative mitochondrial proteomics of the wild-type and virus-infected strains of the chestnut blight fungus. Our data show that hypovirus infection increases the total number of mitochondria, lowers the general ROS level, but increases the mitochondrial respiratory efficiency. Quantification of mitochondrial proteomes revealed that a set of proteins functioning in energy metabolism and mitochondrial morphogenesis as well as virulence were regulated by the virus.
2023-10-24 | PXD041756 | Pride
Project description:A putative homologue of the Saccharomyces cerevisiae Ste12 transcription factor was identified in a series of expressed sequence tag (EST)-based microarray analyses as being down regulated in strains of the chestnut blight fungus, Cryphonectria parasitica, infected by virulence-attenuating hypoviruses. Cloning of the corresponding gene, cpst12, confirmed a high level of similarity to Ste12 homologues of other filamentous fungi. Disruption of cpst12 resulted in no alterations in in vitro growth characteristics or colony morphology and an increase in the production of asexual spores, indicating that CpST12 is dispensable for vegetative growth and conidiation on artificial medium. However, the disruption mutants showed a very substantial reduction in virulence on chestnut tissue and a complete loss of female fertility, two symptoms normally conferred by hypovirus infection. Both virulence and female fertility were restored by complementation with the wild-type cpst12 gene. Analysis of transcriptional changes caused by cpst12 gene disruption with a custom C. parastica cDNA microaray chip identified 152 responsive genes. A significant number of these putative CpST12-regulated genes were also responsive to hypovirus infection. Thus, cpst12 encodes a cellular transcription factor, CpST12, that is down-regulated by hypovirus infection and required for female fertility, virulence and regulated expression of a subset of hypovirus responsive host genes. Keywords: Genetic modification
2006-11-30 | GSE6371 | GEO
Project description:The underlying molecular mechanisms of programmed cell death (PCD) associated with fungal allorecognition, a form of innate immunity, remain largely unknown. In this study, transcriptome analysis was used to infer mechanisms activated during barrage formation in vic3-incompatible strains of C. parasitica, the chestnut blight fungus. Pronounced differential expression occurred in barraging strains of genes involved in mating pheromone (mf2-1, mf2-2), secondary metabolite production, detoxification (including oxidative stress), apoptosis-related, RNA interference and HET-domain genes. Evidence for secondary metabolite production and reactive oxygen species (ROS) accumulation is supported through UPLC-HRMS analysis and cytological staining, respectively. Differential expression of mating-related genes and HET-domain genes was further examined by RT-qPCR of incompatible interactions involving each of the 6 vegetative incompatibility (vic) loci in C. parasitica and revealed distinct recognition process networks. We infer that vegetative incompatibility in C. parasitica activates defence reactions that involve secondary metabolism, resulting in increased toxicity of the extra- and intracellular environment. Accumulation of ROS (and other potential toxins) may result in detoxification failure and activation of apoptosis, sporulation, and the expression of associated pheromone genes. The incompatible reaction leaves abundant traces of a process-specific metabolome as conidiation is initiated.
2020-09-30 | GSE158756 | GEO
Project description:Infection of the chestnut blight fungus, Cryphonectria parasitica, by hypovirus CHV1-EP713 or by reoviruses 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. CHV1-EP713 infection results in depressed pigmentation and conidiation while reovirus infection has little effect on these processes. We now report that loss of female fertility and resulting absence of virus transmission through sexual spores observed after hypovirus infection was not observed for reovirus infected C. parasitica. Reovirus-infected strains were male and female fertile and able to transmit virus to ascospore progeny at a high rate when serving as a female parent. Consistent with this result, real-time RT-PCR revealed that expression of two genes involved in sexual reproduction, the pheromone precursor gene, mf2-1 and yeast Ste12-like transcriptional factor gene, Cpst12, were less reduced in reovirus-infected strains than in hypovirus-infected strains. Analysis with a custom microarray cDNA chip containing EST clones representing ca 2,200 unique C. parasitica genes identified 140 and 128 host genes that were responsive to MYRV1-Cp9B21 and MYRV2-CpC18 infection, respectively. Comparison of these virus-responsive genes revealed an overlap of 85 genes even though the overall degree of nucleotide sequence identity of 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 genes that were responsive to reoviruses MYRV1-Cp9B21 and MYRV2-CpC18 infection were also responsive to CHV1-EP713 infection. Finally, similar to results reported for hypovirus infection, a high percentage (59% and 66%) of the mycoreovirus 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. Keywords: Mycoreovirus, hypovirus, gene expression, microarray.
2007-04-20 | GSE7551 | GEO
Project description:Infection of the chestnut blight fungus, Cryphonectria parasitica, by hypovirus CHV1-EP713 or by reoviruses 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. CHV1-EP713 infection results in depressed pigmentation and conidiation while reovirus infection has little effect on these processes. We now report that loss of female fertility and resulting absence of virus transmission through sexual spores observed after hypovirus infection was not observed for reovirus infected C. parasitica. Reovirus-infected strains were male and female fertile and able to transmit virus to ascospore progeny at a high rate when serving as a female parent. Consistent with this result, real-time RT-PCR revealed that expression of two genes involved in sexual reproduction, the pheromone precursor gene, mf2-1 and yeast Ste12-like transcriptional factor gene, Cpst12, were less reduced in reovirus-infected strains than in hypovirus-infected strains. Analysis with a custom microarray cDNA chip containing EST clones representing ca 2,200 unique C. parasitica genes identified 140 and 128 host genes that were responsive to MYRV1-Cp9B21 and MYRV2-CpC18 infection, respectively. Comparison of these virus-responsive genes revealed an overlap of 85 genes even though the overall degree of nucleotide sequence identity of 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 genes that were responsive to reoviruses MYRV1-Cp9B21 and MYRV2-CpC18 infection were also responsive to CHV1-EP713 infection. Finally, similar to results reported for hypovirus infection, a high percentage (59% and 66%) of the mycoreovirus 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. Keywords: Mycoreovirus, hypovirus, gene expression, microarray.
2007-04-20 | GSE7546 | GEO
Project description:Cryphonectria parasitica infected with PaPlV1
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Project description:Reovirus MyRV2-CpC18 responsive genes in Cryphonectria parasitica
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Project description:Cryphonectria parasitica Genome sequencing
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Project description:Reovirus MyRV1-Cp9B21 responsive genes in Cryphonectria parasitica
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