No description available.

Thesis (M.S. in plant pathology)--Washington State University, May 2009. / Title from PDF title page (viewed on May 22, 2009). "Department of Plant Pathology." Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1956. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 51-52).

M.Sc. / Inducible defence responses in both a susceptible cotton cultivar ( Acala ) and a resistant cotton cultivar ( OR-19 ) in response to elicitors fromVerticillium dahliae were investigated. These oligosaccharin elicitors represent the heat solubilized, non-dialyzable fraction of the pathogen cell wall. This elicitorfraction consist of 6.57 % protein and 68 % carbohydrate and represent merely a discrete portion of the cell wall. Moreover, symptoms such as chlorosis and necrosis were induced by the elicitor in both cultivars, but the timing and magnitute of symptom development differed in that the symptoms occurred much faster and were more intense ( hypersensitive response) in the resistant cultivar. An effective elicitor concentration of 30 ug/ ml ( = 21 ug glucose equivalents) was determined and used throughout this study. Inducible defence responses i.e, the accumulation of PR-proteins and specifically activities of B-1,3-glucanase and chitinase were investigated in the intercellular environment as well as cellular extractions of both cultivars. An attempt was also made to analyse the expression of B-1 ,3-glucanase and chitinase genes at them RNA level ( level of transcription) and to correlate it to the determined levels of enzyme activities. Lignification as well as smaller plant metabolites i.e, sesquiterpenoid-phytoalexins relating to pathogenesis that are induced by the elicitor, were also investigated in both cultivars. In this study it is shown that differences are found between Acala and OR-19 and that some of these differences can be correlated to plant resistance. These differences found in the time studies ( intensity, time of response, qualitative and quantitative differences ) of the defence responses induced in both cultivars is discussed against the background of disease resistance.

D.Sc. (Biochemistry) / Please refer to full text to view abstract

Thesis (M.Sc.)(Plant Biotechnology))--University of Pretoria, 2002. / Summaries in Afrikaans and English. Includes bibliographical references.

This item was digitized as part of the Million Books Project led by Carnegie Mellon University and supported by grants from the National Science Foundation (NSF). Cornell University coordinated the participation of land-grant and agricultural libraries in providing historical agricultural information for the digitization project; the University of Arizona Libraries, the College of Agriculture and Life Sciences, and the Office of Arid Lands Studies collaborated in the selection and provision of material for the digitization project.

No description available.

Verticillium wilt, caused by the soil-borne Verticillium dahliae Klebahn is a serious problem in the production of sunflower worldwide. To date, information on sunflower resistance to Verticillium spp. is very scarce, although it is critical for an effective management of this pathogen. In this study, two highly aggressive (Vd1396-9 and Vd1398-21) and two weakly aggressive V. dahliae isolates (Vs06-07 and Vs06-14) were used to inoculate moderately resistant (IS6111) and susceptible (IS8048) sunflower hybrids. VdNEP (V. dahliae necrosis and ethylene-inducing protein), an elicitor from V. dahliae, was also used to infiltrate sunflower plants. Our results indicate that VdNEP has a dual role in the interaction between sunflower and V. dahliae. VdNEP acted not only as a pathogenicity factor on sunflower by inducing wilting symptoms such as chlorosis, necrosis and vascular discoloration, but also as an elicitor triggering defense responses of the host. VdNEP induced the hypersensitive cell death in Nicotiana benthamiana leaves and sunflower cotyledons. Moreover, VdNEP activated the production of reactive oxygen species and the accumulation of fluorescent compounds in sunflower leaves. Pathogenesis-related genes (Ha-PR-3, and Ha-PR-5), two defensin genes (Ha-PDF and Ha-CUA1) and genes encoding Ha-ACO, Ha-CHOX, Ha-GST and Ha-SCO were up-regulated by VdNEP, suggesting that multiple signaling pathways are involved in this interaction. Two SA-related genes (Ha-PAL and Ha-NML1) were slightly suppressed after infiltration with VdNEP, suggesting a possible involvement of VdNEP in affecting sunflower defenses.

Verticillium wilt, caused by the soil-borne Verticillium dahliae Klebahn is a serious problem in the production of sunflower worldwide. To date, information on sunflower resistance to Verticillium spp. is very scarce, although it is critical for an effective management of this pathogen. In this study, two highly aggressive (Vd1396-9 and Vd1398-21) and two weakly aggressive V. dahliae isolates (Vs06-07 and Vs06-14) were used to inoculate moderately resistant (IS6111) and susceptible (IS8048) sunflower hybrids. VdNEP (V. dahliae necrosis and ethylene-inducing protein), an elicitor from V. dahliae, was also used to infiltrate sunflower plants. Our results indicate that VdNEP has a dual role in the interaction between sunflower and V. dahliae. VdNEP acted not only as a pathogenicity factor on sunflower by inducing wilting symptoms such as chlorosis, necrosis and vascular discoloration, but also as an elicitor triggering defense responses of the host. VdNEP induced the hypersensitive cell death in Nicotiana benthamiana leaves and sunflower cotyledons. Moreover, VdNEP activated the production of reactive oxygen species and the accumulation of fluorescent compounds in sunflower leaves. Pathogenesis-related genes (Ha-PR-3, and Ha-PR-5), two defensin genes (Ha-PDF and Ha-CUA1) and genes encoding Ha-ACO, Ha-CHOX, Ha-GST and Ha-SCO were up-regulated by VdNEP, suggesting that multiple signaling pathways are involved in this interaction. Two SA-related genes (Ha-PAL and Ha-NML1) were slightly suppressed after infiltration with VdNEP, suggesting a possible involvement of VdNEP in affecting sunflower defenses.