Call number: LD2668 .T4 1953 S75 / Master of Science

Call number: LD2668 .T4 1964 D32 / Master of Science

No description available.

No description available.

Typescript. / Thesis (Ph. D.)--University of Hawaii, 1963. / Bibliography: leaves 67-71. / v, 71, [3] leaves mount. illus. (part col.) mount. diagrs., tables

Typescript, etc.

Solanum lycopersicon (the cultivated tomato) is a commodity of great economic importance in South Africa (SA) as well as worldwide. A destructive viral disease known as Tomato curly stunt virus, ToCSV-[ZA:Ond:98], belonging to the genus Begomovirus has negatively impacted on tomato production in SA. This has brought about the need to develop resistant cultivars to ToCSV. Since all cultivated tomato cultivars are susceptible to ToCSV, resistance genes against the virus found in wild tomato plant species have been introgressed into the cultivated tomato by plant breeding techniques. Wild relatives of tomato were adapted to many pathogens (including viruses) as well as stresses from the surrounding environment. During breeding for improved fruit quality and increased yield, the gene networks giving rise to many biotic and abiotic stress resistances have been lost leaving the domesticated tomato extremely susceptible. Plant breeders have reconstituted some of the gene networks into the cultivated tomato that provide tolerance to stresses including viruses. They have achieved this by the help of marker-assisted selection (MAS), where the associated marker is used as an indirect selection criterion. This is an important process in commercial breeding programs as it allows for a speedy selection of selected traits in the development of tomato hybrids. The defence response to abiotic stresses in plants includes the expression of heat shock proteins (HSPs) that function as stress response proteins, molecular chaperones and proteases which repair or degrade damaged proteins. The objective of this study was to elucidate the type of resistance mechanism of a tomato inbred line (TAM), to ToCSV. Since TYLCV-IL shows 77% nucleotide identity with ToCSV, molecular markers already established for the detection of resistance genes for TYLCV-IL were used to screen TAM. The inbred line, TAM, was screened for the absence of any of the known resistant genes to TYLCV-IL using molecular markers already established for the screening of TYCLV-IL resistance genes. TAM was crossed with susceptible cultivar, Rooikhaki, to produce F1 hybrids. These F1 hybrids were selfed to produce an F2 population. Infection trials using ToCSV were conducted using TAM inbred line, F1 hybrids and the F2 population. Since TAM did not have any of the known resistance genes to TYLCV-IL, a possible novel resistance source to ToCSV was speculated. A clue to the resistant mechanism against ToCSV resistance in TAM was indicated by the segregation patterns of the F2 population after inoculation with ToCSV. The results suggest that the resistance is under the control of partially dominant resistant genes. The level of resistance of commercial South African tomato cultivars (Tyler and Tovi-star) against TYLCV-IL was investigated. The heat shock protein (HSP) profiles of these two SA lines including susceptible cultivar, Rooikhaki, were treated with abiotic stresses (salt and heat) and results were compared with a similar study conducted with TYCLV-IL resistant and susceptible tomato cultivars. Heat shock protein 70 accumulation patterns were similar in that HSP70 was more stable in the resistant cultivars throughout the application when abiotic stresses were applied to the SA resistant and susceptible tomato cultivars as compared to Israel resistant and susceptible breeding lines. A relation between infection severity and the pattern of HSP expression was found. A higher level of HSP 70 in resistant tomato plants could contribute to a lower symptom severity phenotype.

Vita. / Digitized by Kansas Correctional Industries

INTRODUCTION In the summer of 1918, at Blacksburg, Virginia, there developed a considerable amount of a soft rot of tomatoes. This occurred in experimental plots which were designated to study the control of septoria leaf blight, and the soft rot of the fruit developed into an important factor. In describing these experiments Fromme (2) states: "Practically all of the unsoundness of the fruit was caused by bacterial soft rot, a disease which is exceedingly common and often very destructive in tomato fields in Virginia." Isolations from diseased fruits made by S. A. Wingard proved a bacterium to be the causative agent. Its growth in pure culture resembled that of the group of bacteria which causes soft rots of plants but it could not be readily assigned to any of the described species of this group. There has been only casual mention of a bacterial soft rot of tomato in literature, and the distinguishing features of the organisms which might be responsible have not been as sharply defined as is desirable. It was decided, therefore, to undertake comparative studies of the organism in question together with some of the non-chromogenic soft rot forms. / Master of Science

Ph.D. / In plants, salicylic acid (SA) is a signaling molecule that regulates disease resistance responses such as systemic acquired resistance (SAR) and the hypersensitive response (HR), and has been implicated in both basal and acquired thermotolerance. It has also been shown that SA enhances heat-induced Hsp/Hsc70 accumulation in plants. In this study, temperature studies revealed that heat shock (HS) at 40 °C for 30 min significantly induced Hsp/Hsc70 accumulation in 3-week old tomato (UC82B) seedlings. Time- and dose-responsive studies showed that 0.1 mM SA for 17 hrs was unable to induce Hsp/Hsc70 but in combination with HS significantly (P > 0.001) potentiated this response. To investigate the mechanism of SA-mediated, heat-induced Hsp/Hsc70 potentiation, tomato seedlings were treated with either SA alone, HS or both, before analyses of hsp70 mRNA, Hsf DNA-binding and gene expression of hsp70, hsfAl, hsfA2 and hsfEll. SA alone established Hsf DNA-binding, but was not accompanied by increased Hsp70 accumulation or expression of hsp70 mRNA. SA had no significant effect on hsfA2 and hsf81 gene expression, but increased the basal levels of hsfAl. In heat-shocked plants, Hsf DNA-binding was enhanced, and increased hsfAl, hsfA2 and hsfB1 expression preceded accumulation of Hsp70. The combined treatment of SA and HS resulted in potentiated Hsf DNA-binding, enhanced expression of hsp70, hsfAl, hsfA2 and hsfB1, leading to potentiated levels of Hsp/Hsc70. Since increased hsp70 and hsf gene expression coincided with increased levels of Hsp70 accumulation, it is likely that the SA-mediated potentiation of Hsp70 is due to the ability of SA to regulate Hsfs during HS. This study therefore proposes a mechanism for the potentiation of Hsp70 by SA in the presence of heat, which might contribute to our understanding of the role SA plays in the heat shock response and thermotolerance.