Developmental Histopathology of Cankers Incited by Hypovirulent and Virulent Isolates of<i>Endothia parasitica</i>on Susceptible and Resistant Chestnut Trees

Hebard, Frederick V.; Griffin, G. J.; Elkins, J. R.

doi:10.1094/phyto-74-140

Cited by 71 publications

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“…Infection by C. parasitica does not involve the formation of specialized infection structures. Colonization of wound sites is followed by the formation of parallel arrays of hyphae called a mycelial fan that effectively penetrates host wound periderm and lignified zones deposited by the host to confine the invading hyphae (23). The apparent similarities in roles for Ste12 homologues for invasive pathogenic growth by plant pathogenic fungi with quite different infection strategies and plant hosts deserves further comparative studies.…”

Section: Discussionmentioning

confidence: 99%

Ste12 Transcription Factor Homologue CpST12 Is Down-Regulated by HypovirusInfection and Required for Virulence and Female Fertility of the Chestnut Blight Fungus Cryphonectria parasitica

2007

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A putative homologue of the Saccharomyces cerevisiae Ste12 transcription factor was identified in a series of expressed sequence tag-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.Hypovirus infection of the chestnut blight fungus Cryphonectria parasitica results in a persistent and stable set of phenotypic changes that can include reduced pigmentation, suppressed asexual sporulation, loss of female fertility, and hypovirulence (reduced virulence) (recently reviewed in references 17 and 32). The pleiotropic nature of these phenotypic changes suggested that hypoviruses may perturb one or several cellular regulatory pathways. Consistent with this view, a series of studies have provided evidence that hypovirus infection alters G-protein-linked, cyclic AMP-mediated (9, 10, 21, 36) and calcium/calmodulin/inositol trisphosphate-dependent (26, 27) signaling cascades, as well as a mitogen-activated protein kinase (MAPK) signaling pathway (35).The development of an expressed sequence tag (EST)-based microarray representing approximately 2,200 C. parasitica genes has provided the means to monitor transcriptional responses to hypovirus infection and to the disruption of specific cellular signaling pathways. Infection by the prototypic hypovirus CHV1-EP713 was shown to result in the modulation of ca. 13.4% of the C. parasitica transcriptome, representing a broad spectrum of biological functions, including stress responses, carbon metabolism, and transcriptional regulation (1). In similar analyses of C. parasitica strains deleted for the G␣ subunit gene cpg-1 and the G␤ subunit gene cpgb-1, respectively, more than 250 C. parasitica genes that are potentially regulated by G-protein signaling were identified (19). Comparisons of transcriptional profiles revealed that more ...

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Section: Discussionmentioning

confidence: 99%

Ste12 Transcription Factor Homologue CpST12 Is Down-Regulated by HypovirusInfection and Required for Virulence and Female Fertility of the Chestnut Blight Fungus Cryphonectria parasitica

2007

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“…This fungus enters the tree through wounds and, in the process of colonizing the wound, forms a hyphal fan with which the fungus invades healthy tissues (11). After colonizing the bark tissues, a stroma is formed directly beneath the outermost layer of bark, which is comprised of a combination of dead and dying tree tissues and fungal hyphae.…”

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confidence: 99%

A Hydrophobin of the Chestnut Blight Fungus, Cryphonectria parasitica , Is Required for Stromal Pustule Eruption

Kazmierczak

Kim

Turina³

et al. 2005

Eukaryot Cell

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Hydrophobins are abundant small hydrophobic proteins that are present on the surfaces of many filamentous fungi. The chestnut blight pathogen Cryphonectria parasitica was shown to produce a class II hydrophobin, cryparin. Cryparin is the most abundant protein produced by this fungus when grown in liquid culture. When the fungus is growing on chestnut trees, cryparin is found only in the fungal fruiting body walls. Deletion of the gene encoding cryparin resulted in a culture phenotype typical of hydrophobin deletion mutants of other fungi, i.e., easily wettable (nonhydrophobic) hyphae. When grown on the natural substrate of the fungus, however, cryparin-null mutation strains were unable to normally produce its fungal fruiting bodies. Although the stromal pustules showed normal development initially, they were unable to erupt through the bark of the tree. The hydrophobin cryparin thus plays an essential role in the fitness of this important plant pathogen by facilitating the eruption of the fungal fruiting bodies through the bark of its host tree.The exterior surfaces of plants are formidable barriers to pathogens. Most plant pathogens are unable to directly penetrate these barriers, and those that can penetrate these barriers have evolved remarkable strategies for doing so. For example, Plasmodiophora brassicae (1) penetrates the host wall by puncturing it with a specialized structure called the stachel. Magnaporthe grisea, the rice blast pathogen, produces another type of specialized structure, the appressorium, which penetrates the plant cuticle with a peg that develops unusually high hydrostatic pressures (26). To exit a plant, the same barriers that met the pathogen on entry must once again be crossed. Some pathogens, such as the late-blight pathogen Phytophthora infestans, sporulate by exiting natural openings on the plant surface. Little is known, however, of how those fungi that sporulate by erupting through host tissues are able to breach the plant surface barriers. It is known that microbial pathogens must be able to exit their hosts and gain access to new hosts in order to successfully complete the disease cycle.The search for pathogenicity factors of fungal plant pathogens has focused largely upon understanding how the fungus invades its host (8,13,20,29). Much less attention has been paid to the role of sporulation as a potential target for control of disease. From our study of cryparin, a cell surface hydrophobin of the plant pathogen Cryphonectria parasitica, we report the involvement of this protein in the normal egress of the fungus from infected trees. This protein thus acts as a pathogenicity factor since it is necessary for the successful completion of the pathogen's disease cycle.The ascomycete C. parasitica is one of the most devastating plant pathogens of recorded history; it has essentially eliminated its host, the American chestnut, from its natural range. This fungus enters the tree through wounds and, in the process of colonizing the wound, forms a hyphal fan with which the fungus invade...

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“…One potential explanation for the species-specific responses to JA and its inhibitor may be found in the context of species-specific responses to infection by the chestnut blight fungus. The blight fungus causes cankers on susceptible chestnut stems by destroying vascular tissues (Hebard et al 1984), and JA synthesis increases following tissue damage and water stress (reviewed by Creelman and Mullet 1997;Schilmiller and Howe 2005). The American chestnut is highly susceptible to the blight fungus, and those used in this study were infected.…”

Section: Discussionmentioning

confidence: 99%

Woody Stem Galls Interact With Foliage to Affect Community Associations

Cooper

Rieske

2009

Environ Entomol

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Developmental Histopathology of Cankers Incited by Hypovirulent and Virulent Isolates ofEndothia parasiticaon Susceptible and Resistant Chestnut Trees

Cited by 71 publications

References 0 publications

Ste12 Transcription Factor Homologue CpST12 Is Down-Regulated by HypovirusInfection and Required for Virulence and Female Fertility of the Chestnut Blight Fungus Cryphonectria parasitica

Ste12 Transcription Factor Homologue CpST12 Is Down-Regulated by HypovirusInfection and Required for Virulence and Female Fertility of the Chestnut Blight Fungus Cryphonectria parasitica

A Hydrophobin of the Chestnut Blight Fungus, Cryphonectria parasitica , Is Required for Stromal Pustule Eruption

Woody Stem Galls Interact With Foliage to Affect Community Associations

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