Browsing by Author "Taylor, Christine Helen"
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- ItemStudies of camellia flower blight (Ciborinia camelliae Kohn) : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Plant Science (Plant Pathology) at Massey University, Palmerston North, New Zealand(Massey University, 2004) Taylor, Christine HelenCamellias are popular ornamental plants and the most serious pathogen of this plant is camellia flower blight, caused by the fungal pathogen Ciborinia camelliae Kohn. Ascospores of this fungus attack the flowers, turning them brown, rendering infected flowers unattractive. Little is known about the pathogen and control measures are not particularly effective. In this thesis, various aspects of the pathogen's basic and molecular biology and interaction with host species were studied. Surveys of the distribution and spread of C. camelliae within New Zealand determined that the pathogen was present in most regions of the North Island, and north and east coasts of the South Island. Over the distances and time involved, it appeared that the disease was spreading mainly by windborne ascospores rather than human transfer. Sclerotia were germinated out of season to increase the period during which ascospores were available for infection work. Greatest germination was achieved at low temperatures (5°C-10°C) in 24 h darkness. Isolate-specific primers were designed to the ribosomal DNA Internal Transcribed Spacer region to detect the pathogen in planta and distinguish between New Zealand isolates of C. camelliae and other fungal pathogens. Phylogenetic analysis of the ITS region with other Ciborinia, Sclerotinia and Botrytis species showed that C. camelliae was more closely related to S. sclerotiorum than other Ciborinia species. Two inoculation techniques for infecting Camellia petals with ascospores of C. camelliae were developed and tested. Inoculation using airborne ascospores in a settling chamber was a simple and quick method for testing large numbers of species for resistance. Inoculation of ascospores in suspension produced qualitative data, but was more time consuming. Of the four mechanisms of resistance tested, levels of aluminium hyperaccumulation and the presence of phenolic compounds did not correlate with resistance in Camellia species. The large uptake of aluminium, however, did indicate that Camellia species would be good plants for phytoremediation of acid soils. Some resistant species were found to have cell wall modifications and/or lignification of cell walls in response to C. camelliae infection and chitinase activity was found in most resistant Camellia species tested. Further research into these latter two mechanisms is recommended and indicates that the development of resistant Camellia cultivars is possible.
- ItemStudies of camellia flower blight (Ciborinia camelliae) : a thesis presented in partial fulfilment of the requirements for the degree of Master of Applied Science in Plant Health at Massey University(Massey University, 1999) Taylor, Christine HelenCamellias are popular ornamental plants grown for their verdant evergreen foliage and spectacular flowers, which come in many colours, sizes and forms. The fungal pathogen (Ciborinia camelliae), which causes camellia flower blight, is considered the most serious disease of the camellia genus as it attacks the flowers, causing them to turn brown and fall early. The pathogen was described in Japan in 1919, spread to the USA in 1938 and was discovered in New Zealand in 1993. Relatively little research has been done on the pathogen or the disease that it causes. Chemical and cultural control methods have not proved particularly effective. The fungus was isolated from sclerotial medulla and isolates grew significantly better on Camellia Petal PDA, Oxoid PDA, Difco PDA and Oxoid MEA than on Homemade PDA, expired Oxoid PDA and Merck PDA. Cultures were maintained on Difco PDA and optimum temperatures for growth and sclerotial formation were between 15°C and 20°C. Surveys of the North Island in 1997 and both North and South Island in 1998 found the pathogen was more widely distributed than previously thought. It is widespread in the central, western and lower North Island and present in the north of the South Island and Christchurch. Although the outbreaks in Auckland and in Christchurch were probably the result of the transfer of infected material, dispersal by windborne ascospores appears to be the main method of spread. Conditions that stimulate sclerotial germination out of season were investigated using both protocols established for other fungi and novel methods that involved incubation at various temperatures, combinations of temperatures, and light. Artificial stimulation of germination was not achieved. Infection of petals was investigated using agar plug inoculation and, during the disease season, ascospores. Wounding was required for infection from plug inoculum but not from ascospores. Younger buds appeared to have more resistance to both types of inoculum. Ascospore inoculations of species and varieties showed that there were levels of resistance within the genus but this was not quantified. Several potential biocontrol agents, effective against the ascospore stage, were isolated but could not be evaluated due to the limited ascospore production season. Further research is required to study the pathogen/host interaction, the infection process, levels of resistance and mechanisms of resistance. Breeding for resistance appears to be possible and offers the best long term prospects for the control of this disease.