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Biology of virulent and hypovirulent Endothia parasitica on American chestnut (Castanea dentata)

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dc.contributor.authorHebard, Frederick Vanuxemen
dc.contributor.committeechairGriffin, Gary J.en
dc.contributor.committeememberElkins, J.R.en
dc.contributor.committeememberAlexander, S.A.en
dc.contributor.committeememberMoore, L.D.en
dc.contributor.committeememberDrake, Charles R.en
dc.contributor.committeememberStipes, R. Jayen
dc.contributor.departmentPlant Pathologyen
dc.date.accessioned2017-03-10T21:56:04Zen
dc.date.available2017-03-10T21:56:04Zen
dc.date.issued1982en
dc.description.abstractResults of inoculations of grafts, seedlings, excised stems, and intact trees of large, surviving American chestnut indicated that some have heritable blight resistance. Some degree of resistance in American chestnut possibly would assist spread of hypovirulence (H) factors. The pathogenicity of the H isolate but not the V (virulent) isolate appeared to influence the size and sporulating characteristics of biocontrolled H+V cankers. The histopathology of canker development on blight-resistant Chinese and blight-resistant and blight-susceptible American chestnut was examined after inoculation with V and H E-parasitica. Rapid formation and continual growth of mycelial fans distinguished chestnut blight cankers incited by V E-parasitica from those incited by H E-parasitica, and distinguished cankers on susceptible chestnut from cankers on resistant chestnut. Differences among such cankers in wound periderm and other pathological alterations of bark and wood anatomy probably were results of differences in rates of fan formation and growth. Wound periderm formation began at the deepest point of a wound or canker and progressed outward to the bark surface. Superficial cankers arose in resistant trees or with hypovirulent fungus when slow-forming mycelial fans expanded through areas where wound periderm had not formed. Rapid epidemics of chestnut blight occur in recently clearcut areas but not in areas with large trees of species other than American chestnut, most probably because chestnut sprouts released after cutting become larger than they do when overtopped by large forest trees. The size of chestnut sprouts appeared to influence the rate of blight progress by setting a maximum limit on canker size and thus canker sporulation. It may be possible to foster spread of H factors in the Appalachians if blight epidemics in clearcuts can be prolonged. This might be done by restricting inoculum production. Cutting and removing some blighted sprouts, cutting some large unblighted sprouts, or increasing blight resistance in the chestnut population are three potential means of restricting inoculum production.en
dc.description.degreePh. D.en
dc.format.extentxii, 295, [2] leavesen
dc.format.mimetypeapplication/pdfen
dc.identifier.urihttp://hdl.handle.net/10919/76589en
dc.language.isoen_USen
dc.publisherVirginia Polytechnic Institute and State Universityen
dc.relation.isformatofOCLC# 8731266en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subject.lccLD5655.V856 1982.H422en
dc.subject.lcshChestnut blighten
dc.subject.lcshAmerican chestnut -- Diseases and pestsen
dc.subject.lcshEndothia parasiticaen
dc.titleBiology of virulent and hypovirulent Endothia parasitica on American chestnut (Castanea dentata)en
dc.typeDissertationen
dc.type.dcmitypeTexten
thesis.degree.disciplinePlant Pathologyen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.namePh. D.en

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