"February 2004" / Bibliography: leaves 150-185. / xiii, 185 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / "This project was designed to investgate new resistant populations of Hordeum spp; to assess the role of gene flow in spreading resistance; to determine the fitness of resistant individuals in accelerating resistance evolution; and to identify genetic relationships between resistant and susceptible populations using DNA markers." / Thesis (Ph.D.)--University of Adelaide, School of Agriculture and Wine, Faculty of Sciences, 2005

Call number: LD2668 .T4 1957 O94 / Master of Science

Includes bibliographical references (l5 leaves) The aim of the work presented in this thesis was to develop molecular genetic markers for YD2 (the gene in barley which provides protection against barley yellow dwarf luteovirus) which could be used for the marker assisted selection of the gene in breeding programs and enable the gene to be cloned via a map-based approach.

Graduation date: 2002

Molecular tools, coupled with unique germplasm stocks and rigorous phenotyping, are useful for developing a better understanding of qualitative and quantitative disease resistance genes in plants. The identification of molecular markers linked to all types of resistance genes provides opportunities for implementing a range of resistance breeding strategies, ranging from gene pyramiding to gene deployment. This thesis consists of two chapters. The first describes a disease resistance gene mapping effort and the second describes a disease resistance gene introgression effort. The number, location, and effects of genes determining resistance to stripe rust, leaf rust and Barley Yellow Dwarf Virus were determined using a population of doubled haploid (DH) lines from the cross of Shyri x Galena. Resistance to leaf rust was qualitatively inherited, and the locus was mapped to the long arm of chromosome 1. Resistance to stripe rust and BYDV was quantitatively inherited. Multiple QTLs were detected for each type of resistance. The principal stripe rust resistance QTL was on the short arm of chromosome 5 and the principal BYDV resistance QTL was on the long arm of chromosome 1, linked in repulsion phase with the leaf rust resistance gene. Additional QTLs and QTL x QTL interactions were detected. The majority of the qualitative and quantitative resistance loci detected in the Shyri x Galena population coincided with Resistance Gene Analog Polymorphisms (RGAPs) mapped in the same population. These RGAPs were based on degenerate primers derived from cloned resistance gene sequence motifs. These associations should be useful for efficient resistance gene mapping and provide an approach for ultimately isolating and describing quantitative and qualitative resistance genes. The second chapter describes a molecular marker assisted selection (MMAS) effort to introgress stripe rust resistance QTLs on chromosomes 4 and 7 into susceptible germplasm. DH lines were derived form a MMAS backcross-one (BC-1) population, extensively phenotyped for stripe rust resistance, and genotyped for the introgressed QTLs and background genome. The resistance QTLs that were introgressed were significant determinants of resistance in the new genetic background. Additional resistance QTLs were also detected. Together, these chapters describe an integrated approach to disease resistance gene characterization and utilization. / Graduation date: 1999

An evaluation of nineteen barley lines using three artificial inoculation methods concluded that spray inoculation was the most reproducible method and provided the greatest discrimination of resistance. Six of the nineteen barley lines were used for proteomic studies to identify defense responses following F. graminearum infection. All lines responded by inducing an oxidative burst and pathogenesis-related proteins. Differences in response magnitude and the proteins activated could be attributed to varying levels of FHB resistance amongst the barley lines. RNA microarray profiling and iTRAQ technology were used to study the interaction between two barley lines under five different treatments testing the effect of the fungus, trichothecene, and their interaction. Resistance was differentiated by the early induction of defense-related genes and the activation of the JA and ethylene defense pathways in Chevron, compared to the induction of a less efficient defense pathway in Stander; observed intra- and inter-cultivar differential responses are discussed. / xvii, 196 leaves : ill. ; 29 cm.

Stripe rust (Puccinia striiformis f. sp. hordei) is a serious disease of barley that can cause up to 70% yield loss in susceptible varieties. The fungus is moving northward, threatening major barley production areas in the US, where most cultivars are susceptible. Fungicides are available for control of stripe rust, but economic and environmental considerations favor genetic resistance. Two stripe rust resistance quantitative trait loci (QTLs) located in chromosomes 4 and 7 have previously been reported. One hundred and ten doubled haploid progeny from a stripe rust susceptible x resistant cross were derived using the Hordeum bulbosum technique and phenotyped for agronomic and malting quality traits in order to assess the importance of linkage drag associated with the mapped stripe rust resistance QTLs. Data on 33 markers were combined with phenotypic data for QTL analysis. A molecular marker-assisted backcross program was implemented to initiate the transfer of the stripe rust resistance loci into susceptible US germplasm. No negative QTLs for agronomic or malting quality traits were detected within or adjacent to the intervals that were targeted for marker-assisted selection. A minor leaf rust resistance QTL, however, was found adjacent to the stripe rust locus on chromosome 7. Linkage drag in this region could operate in favor of the breeder. Epistatic interaction between the two stripe rust resistance QTLs confirms the necessity of introgressing both chromosome intervals. / Graduation date: 1994

The linkage relationship and arm location of the gene for greenbug resistance in the variety Will was determined by using primary trisonomics and tertiary trisomic homozygous translocations. The gene for greenbug resistance was found to be on linkage group 1 by using primary trisonomics. The gene was located on the cetromere segment of the Tl-6a translocation by using a tertiary trismoic homozygous for greenbug resistance. The data further substantiates the feasibility of using trisomics in placing genes on proper linkage groups.

Conventional linkage and primary trisomic analyses were undertaken to locate genes conditioning resistance of barley (Hordeum vulgare L.) to Puccinia hordei Otth. The linkage relationships of resistance genes Pa in Speciale (C.I. 7536) and Pa₇ in Cebada Capa (C.I. 6193) with genes known to reside on chromosomes 2 and 3 were studied in crosses involving Speciale and three chromosome 2 markers (e, gs₅, and lr), and in crosses involving Cebada Capa and four chromosome 3 markers (gs₂, uz, als, and yst₂). The location of the resistance gene Pa₃ in Estate was studied by primary trisomic analysis. Inheritance of leaf rust resistance was determined by seedling reaction to culture 57-19, race UN4 of Puccinia hordei. The inheritance and linkage relationships of marker genes and rust resistance were analyzed from F₂ and F₃ coupling data. A recombination value of 41.0 ± 2.2% was found between Pa and gs₅, a marker for chromosome 2L. No evidence was obtained linking Pa with genes e or lr, but population sizes were too small to detect reliably loose linkages in these populations. A loose association was observed between Pa₇ and yst₂ a marker for chromosome 3S; however, the data were not sufficiently homogeneous to permit estimation of a recombination value. The data from crosses involving Pa₇ and uz were not consistent but one population exhibited a trend which suggested these genes might be linked. No evidence of linkage was observed in crosses between Pa₇ and the genes gs₂ and als, although population sizes were limited. The assignment of Pa₇ to chromosome 3 was confirmed by primary trisomic analyses. By the same method, the Pa₃ gene in Estate was shown to be independent of chromosome 3. High temperatures during leaf rust inoculation and incubation periods resulted in poor expression of infection type in crosses involving Estate and Triplo 4, 5, and 6. Despite this the data from these crosses indicated that Pa₃ is not likely inherited through chromosomes 4 through 6. Accrued data suggest that Pa₃ may be located on chromosome 1. / Ph. D.

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