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Has files: YesSubject: search.filters.subject.Sclerotinia sclerotiorum

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    Characterisation of the cell death-inducing activity of the conserved family of Ciborinia camelliae-like small secreted proteins (CCL-SSPs) of C. camelliae, Botrytis cinerea and Sclerotinia sclerotiorum : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Plant Biology at Massey University, Manawatu, New Zealand
    (Massey University, 2019) McCarthy, Hannah
    Ciborinia camelliae, the causal agent of Camellia petal blight, is a necrotrophic fungus that sequesters nutrients from dead plant cells. Candidate effector proteins have been identified from the secretome as a highly conserved clade, termed C. camelliae-like small secreted proteins (CCL-SSPs). Notably, the CCL-SSPs are not unique to C. camelliae. Indeed, a single homolog of the CCL-SSP family has shown to be encoded by the genomes of the closely related necrotrophs, Botrytis cinerea and Sclerotinia sclerotiorum, (BcSSP and SsSSP, respectively). Previous work has identified the ability of BcSSP and SsSSP to induce cell death on Camellia ‘Nicky Crisp’ petals, whereas of the ten C. camellia CCL-SSPs (CcSSPs) tested, only one induced very weak cell death. The aim of this study was to determine what specific regions of the SsSSP protein confered cell death-inducing ability, and to further characterise the cell death-inducing capability of these CCL-SSPs. In this study it was shown, through generation of chimeric regionswapped proteins and infiltration into Camellia ‘Nicky Crisp’ petals and Nicotiana benthamiana leaves, that the region encoded by Exon 2 of SsSSP is essential for cell death-inducing activity. It was also discovered that BcSSP and SsSSP may induce cell death to different extents, as a significant different was shown in quantified cell death induced on Camellia ‘Nicky Crisp’ petals. It was also found that BcSSP can induce strong cell death on Arabidopsis thaliana leaves, while SsSSP does not. This research also investigated appropriate methods for characterising cell death of CCL-SSPs, and suggested addition of a C-terminus tag for future work. The results of this study have shed further light on the CCL-SSP family as candidate effector proteins and provided several avenues for future researchers to fully elucidate the function of CCL-SSPs and their role in virulence of these three necrotrophic fungi.
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    Epidemiology and management of Sclerotinia sclerotiorum (Lib.) de Bary in kiwifruit (Actinidia deliciosa (A. Chev.)) : this thesis is presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Plant Science at Massey University, Palmerston North, New Zealand
    (Massey University, 2001) Hoyte, Stephen
    Kiwifruit (Actinidia deliciosa (A. Chev.) C. F. Liang et A. R. Ferguson, var. deliciosa cv. „Hayward?), a valuable fruit grown in New Zealand orchards for export, is susceptible to the necrotrophic and cosmopolitan fungus Sclerotinia sclerotiorum (Lib.) de Bary. Sclerotinia disease causes direct crop loss in the form of diseased fruitlets, scarring of fruit and field rot of fruit. Costs to the industry amounting to an estimated $5 million pa. are incurred through crop loss on vines or during grading and through the purchase and application of fungicide. This study showed that 19% (range 0–53%) of 3–4 day-old kiwifruit petals were colonised by S. sclerotiorum ascospores arising from apothecia that were present within most orchards. Adhering floral tissues (AFT) were present on 38% of fruit 7–8 weeks after anthesis and 11% (range 0–43%) of these were colonised by S. sclerotiorum. The incidence of fruit with scarring was significantly higher on fruit with AFT than fruit without AFT. Removal of AFT 10–14 days after anthesis resulted in a 66% reduction in diseased fruitlets and a 85% reduction in fruit with scarring. Adhering floral tissues on fruit were therefore determined to be a major source of secondary spread. An in vitro assay was developed in which freshly detached kiwifruit petals were inoculated with dry S. sclerotiorum ascospores in a settling chamber and incubated for 72 h. The number of discrete colonies which formed on selective agar medium, when macerated petal tissue was spread on the agar, effectively quantified petal colonisation. Colonisation of petals significantly increased with increasing flower age. Colonisation of petals incubated under static conditions within saturated salt chambers was highest between 18–27oC and 90–100% relative humidity. Colonisation of petals in dynamically controlled environment chambers was inhibited by incubation in diurnally fluctuating temperature and relative humidity conditions typical of days with <5 mm rainfall during flowering. The minimum, maximum and optimum temperatures for mycelial growth on PDA and percentage germination of ascospores on water agar (5oC, 34oC and 23oC respectively) were similar to those for the rate of colonisation of petals by ascospores at 100% RH. Symptoms of diseased fruitlets, fruit scarring and field rot were reproduced in field inoculation experiments, provided free moisture was present for at least 9 h. Sclerotia iii were extracted from diseased fruitlets and fruit with field rot from three vines, yielding 2.7 and 18.6 sclerotia per unit respectively. Diseased fruitlets produced significantly smaller sclerotia, which had a higher germination rate and produced smaller apothecia, compared with sclerotia from fruit with field rot. External damage on 39% of sclerotia from fruit with field rot and their closer contact with soil micro-organisms during formation and maturation are likely causes for these observed differences in germination rate. Thus, the type of symptom which develops on pistillate vines can affect the potential for ascospore production during subsequent seasons through the production of ecologically distinct populations of sclerotia. During field studies in 18 orchards, positive relationships were shown between primary inoculum source (apothecial density) and primary infection (incidence of petal colonisation) and between both these factors and the incidence of diseased fruitlets and fruit with scarring. A conceptual model of inoculum production and disease development was constructed. This model highlights the importance of primary colonisation of floral tissues and showed that disease risk can be estimated from the apothecial density or the colonisation of petals by S. sclerotiorum. Model structures have also been developed for predicting disease risk and disease incidence. Disease management strategies are discussed, and if implemented, would rationalise decision processes and potentially reduce the costs of controlling sclerotinia. Decision support software could be developed to incorporate such models once they are validated and combined with further research to determine effective control measures. This software could then be integrated into a sclerotinia management system for kiwifruit in New Zealand.