[Truncated abstract] The genetics of ascochyta blight resistance was studied in five 5 x 5 half-diallel cross sets involving seven genotypes of chickpea (ICC 3996, Almaz, Lasseter, Kaniva, 24B-Isoline, IG 9337 and Kimberley Large), three accessions of Cicer reticulatum (ILWC 118, ILWC 139 and ILWC 184) and one accession of C. echinospermum (ILWC 181) under field conditions. Both F1 and F2 generations were used in the diallel analysis. Almaz, ICC 3996 and ILWC 118 were the most resistant genotypes. Estimates of genetic parameters, following Hayman's method, showed significant additive and dominant gene actions. The analysis also revealed the involvement of both major and minor genes. Susceptibility was dominant over resistance to ascochyta blight. The recessive alleles were concentrated in the two resistant chickpea parents ICC 3996 and Almaz, and one C. reticulatum genotype ILWC 118. High narrow-sense heritability (ranging from 82 to 86% for F1 generations, and 43 to 63% for F2 generations) indicates that additive gene effects were more important than non-additive gene effects in the inheritance of the trait and greater genetic gain by breeding resistant chickpea cultivars using carefully selected parental genotypes. Current simple leaf varieties are often susceptible to ascochyta blight disease whereas varieties of other leaf types range from resistant to susceptible. The inheritance of ascochyta blight resistance and different leaf types and their correlation were investigated in intraspecific progeny derived from crosses among two resistant genotypes with normal leaf type (ICC 3996 and Almaz), one susceptible simple leaf type (Kimberley Large) and one susceptible multipinnate leaf type (24 B-Isoline). ... An interspecific F2 mapping population derived from a cross between chickpea accession ICC 3996 (resistant to ascochyta blight, early flowering, and semi-erect plant growth habit) and C. reticulatum accession ILWC 184 (susceptible to ascochyta blight, ii late flowering, and prostrate plant growth habit) was used for constructing a genetic linkage map. F2 plants were cloned through stem cuttings taken at pre-flowering stage, treated with plant growth regulator powder (0.5 mg/g indole butyric acid (IBA) and 0.5 mg/g naphthalene acetic acid (NAA)) and grown in a sand + potting mix substrate. Clones were screened for ascochyta blight resistance in controlled environment conditions using a 19 scale. Three quantitative trait loci (QTLs) were found for ascochyta blight resistance in this population. Two linked QTLs, located on linkage group (LG) 4, explained 21.1% and 4.9% of the phenotypic variation. The other QTL, located on LG3, explained 22.7% of the phenotypic variation for ascochyta blight resistance. These QTLs explained almost 49% of the variation for ascochyta blight resistance. LG3 had two major QTLs for days to flowering (explaining 90.2% of phenotypic variation) and a major single QTL for plant growth habit (explaining 95.2% of phenotypic variation). There was a negative correlation between ascochyta blight resistance and days to flowering, and a positive correlation between days to flowering and plant growth habit. The flanking markers for ascochyta blight resistance or other morphological characters can be used in marker-assisted selections to facilitate breeding programs.

Thesis (MSc.) -- Stellenbosch University, 1997. / ENGLISH ABSTRACT: An octoploid triticale was derived from the F1 of a Russian wheat aphid resistant rye, 'Turkey 77', and 'Chinese Spring' wheat. The alloploid was crossed (a) to common wheat, and (b) to the 'Imperial' rye to 'Chinese Spring' disomic addition lines. F2 progeny from these crosses were tested for Russian wheat aphid resistance and C-banded. Resistance was found to be associated with chromosome arm 1RS of the 'Turkey 77' rye genome. This initial work was done by MARAIS (1991) who made a RWA resistant, monotelosomic 1RS ('Turkey 77') addition plant available for the study. The F3 progeny of this monotelosomic addition plant was used to confirm the RWA resistance on chromosome 1RS. The monotelosomic addition plant was then crossed with the wheat cultivar 'Gamtoos', which has the 1BL.1 RS 'Veery' translocation. Unlike the 1RS segment in 'Gamtoos', the 'Turkey 77'- derived 1RS telosome did not express the rust resistance genes 5r31 and Lr26 which could then be used as markers. From the F1 a monotelosomic 1RS addition plant that was also heterozygous for the 1BL.1 RS translocation, was selected and testcrossed with an aphid susceptible common wheat, 'Inia 66'. Meiotic pairing between the .rye arms resulted in the recovery of five euploid, Russian wheat aphid resistant plants out of a progeny of 99 euploids. One recombinant also retained 5r31 and Lr26 and was allowed to self pollinate. With the aid of SOS-PAGE profiles, Russian wheat aphid resistant 1BL.1 RS translocation homozygotes were identified and it was possible to confirm that the Russian wheat aphid resistance gene was in fact transferred to the 1BL.1RS ('Veery') translocation. Two attempts were made to map the Russiar, wheat aphid locus or loci. (1) Telosomic mapping was attempted. For this purpose a plant with 2n = 40 + 1BL.1 RS + 1RS was obtained, and testcrossed with a Russian wheat aphid susceptible wheat. (2) A disomic, recombined 1BL.1 RS translocation line with Russian wheat aphid resistance but lacking the Lr26 and Sr31 alleles was crossed with 'Gamtoos' and the F1 testcrossed. The testcross in both strategies were done with 'Chinese Spring'. In the first experiment the Sr31 locus was located 10.42 map units from the Lr26 locus. The rust resistance data implied that the genetic distance estimates may be unreliable and therefore the laborious Russian wheat aphid resistance tests were not done. In the second experiment a Russian wheat aphid resistance gene was located 14.5 map units from the Lr26 locus. In the latter cross nonmendel ian segregation of the Russian wheat aphid resistance evidently occurred which implied that the estimated map distance may be inaccurate. It was also not possible to determine the number of genes involved from the data. / Digitized at 300 dpi Colour & b/W PDF format (OCR), using ,KODAK i 1220 PLUS scanner. Digitised, Ricardo Davids on request from ILL 25 April 2013 / AFRIKAANSE OPSOMMING: 'n Oktaplo"lede triticale is gemaak vanaf die F1 van 'n kruising tussen 'n Russiese koringluis-weerstandbiedende rog, 'Turkey 77', en die koringkultivar 'Chinese Spring'. Die alloplo"led is gekruis met gewone broodkoring en met 'Imperial' rog/'Chinese Spring' disomiese addissielyne. Die F2 nageslag vanaf hierdie kruisings is getoets vir Russiese koringluisweerstandbiedendheid en C-bande is ook gedoen. Weerstand is gevind wat geassosieer is met die 1RS chromosoomarm van 'Turkey 77'. Hierdie oorspronklike werk is deur MARAIS (1991) gedoen en uit sy materiaal is 'n monotelosomiese 1RS ('Turkey 77') addissieplant beskikbaar gestel vir die huidige studie. Die F3 nageslag van hierdie monotelosomiese addissieplant is gebruik om die weerstand teen die Russiese koringluis op chromosoom 1RS te bevestig. Die monotelosomiese addissieplant is ook gekruis met die koringkultivar 'Gamtoos' wat die 1BL.1 RS-translokasie dra. Hoewel die 1RS segment van 'Gamtoos' die roesweerstandsgene, Sr31 en Lr26 uitdruk, is dit nie die geval met die 'Turkey 77' 1RS telosoom nie. Hierdie gene kon dus as merkergene gebruik word. Vanuit die F1 is 'n monotelosomiese 1RS addissieplant geselekteer wat ook heterosigoties was vir die 1BL.1 RStranslokasie. Hierdie plant is getoetskruis met 'n luisvatbare gewone broodkoring, 'Inia 66'. Meiotiese paring tussen die rogarms het daartoe gelei dat vyf euplo"lede Russiese koringluis-weerstandbiedende nageslag uit 99 euplo"lede nageslag geselekteer kon word. Een rekombinant het ook Sr31 en Lr26 behou en is toegelaat om self te bestuif. Met behulp van SDSPAGE profiele is Russiese koringluis-weerstandbiedende 1BL.1 RStranslokasie homosigote ge"ldentifiseer en kon bevestig word dat die weerstandsgeen vir die Russiese koringluis oorgedra is na die 1BL.1 RS ('Veery') -translokasie. Twee strategies is gevolg om die Russiese koringluislokus of -loci te karteer: (1) 'n Telosomiese analise is gedoen. 'n Plant met 2n = 40 + 1BL.1 RS + 1RS is verkry en met 'n luisvatbare koring bestuif. (2) 'n Gerekombineerde, disomiese plant met Russiese koringluis-weerstandbiedendheid maar sonder die Lr26 en Sr31 allele is gekruis met 'Gamtoos' en die F1 getoetskruis. Die toetskruisouer in beide die strategiee was 'Chinese Spring'. In die eerste eksperiment is die Sr31-lokus 10.42 kaarteenhede vanaf die Lr26-lokus gelokaliseer. Die raesdata het ge"impliseer dat onbetraubare genetiese kaarteenhede geskat sou word en daarom is die omslagtige Russiese koringluis weerstandsbepalings nie gedoen nie. In die tweede eksperiment is die Russiese koringluis-weerstandsgeen op 14.5 kaarteenhede vanaf die Lr26-lokus gelokaliseer. Nie-Mendeliese segregasie van die Russiese koringluis-weerstand in hierdie karteringseksperiment het ge'impliseer dat die berekende kaartafstand onakkuraat mag wees. Dit was ook nie moontlik om op grand van die data die aantal gene betrakke af te lei nie.

T. aestivum ssp. spelta Iranian type has long been thought to potentially be the direct non-free threshing hexaploid progenitor. I evaluated a RIL population derived from a cross between CS and Iranian spelta accession P503 to identify loci suppressing free-threshabilty in P503. Identification of QTL associated with threshability in region known to harbor the Tg2A gene, and an inactive tg2D allele supported the hypothesis of Iranian spelta being derived from a more recent hybridization between free-threshing hexaploid and emmer wheat. Parastagonospora nodorum is an important fungal pathogen and secretes necrotrophic effectors that evoke cell death. In this research, a DH population segregating for Snn5 was used to saturate Snn5 region of chromosome 4B with molecular markers. The physical distance between Snn5 flanking markers was narrowed to 1.38 Mb with genetic distance of 2.8 cM. The markers developed in this study will provide a strong foundation for map-based cloning of Snn5.

Call number: LD2668 .T4 1984 C87 / Master of Science

Call number: LD2668 .T4 1985 M43 / Master of Science

Thesis (DMed (Psychiatry))--University of Stellenbosch, 2005. / BACKGROUND Schizophrenia is a heterogeneous disorder, which has been shown to have both environmental and genetic risk factors. Since family history (genetic loading) of psychosis appears to be one of the strongest risk factors for the development of schizophrenia, the investigation of affected sib pairs can be used to explore shared familial factors. The Xhosa-speaking inhabitants in the Western, Eastern and Southern Cape provinces, an African population of relatively homogeneous ethnicity, provided a sample of the first large clinical phenotype of schizophrenia. AIM The main aim of this study was to identify shared symptoms or symptom clusters in a sample of Xhosa-speaking sib pairs, with the aid of structured assessment tools.

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.

In the context of the somatic mutation theory of chemical carcinogenesis, mutations are thought to arise during the replication of DNA past carcinogen-DNA adducts. The work described in this thesis deals with the testing of a hypothetical mechanism whereby mammalian cells are able to replicate their DNA past polycyclic aromatic hydrocarbon DNA adducts. The second objective of this thesis work was to develop both in vivo and in vitro models to study the induction of mutations in a target human gene by chemical carcinogens from two different classes, polycyclic aromatic hydrocarbons and nitrosamines. To approach the hypothetical mechanism of bypass replication in mammalian cells, synchronized Chinese hamster ovary cells were treated with the ultimate carcinogenic form of benzo (a) pyrene, 7β, 8α-dihydroxy-9α, 10α-epoxy-7,8,9,10-tetrahydrobenzo (a) pyrene (BPDE I). Using the pH step alkaline elution assay, it was found that the reduced rate of S phase progression was due to a delay in the appearance of multiple replicon size nascent DNA. It was determined using agarose gel electrophoresis that the ligation of Okazaki size replication intermediates was blocked in BPDE I-treated, synchronized CHO cells. The data obtained were, therefore, supportive of the 'block-gap' model of DNA bypass replication in carcinogen damaged mammalian cells. To study mutagenesis of a specific sequence induced by chemical carcinogens, the human c-Ha-ras proto-oncogene was transfected into the mouse fibroblast cell line, NIH 3T3. Transfected NIH 3T3 cell lines (HHRN 1-4) were isolated that had a low copy number of the human c-Ha-ras proto-oncogene and a non-transformed phenotype. It was determined that the integrated human c-Ha-ras gene was hypomethylated, and expressed at the messenger level. The human c-Ha-ras protein, p21, was also detected in these transfected cell lines. Treatment of the HHRN cell lines with the nitrosamine, N-methyl-N-nitroso-N'-nitroguanidine (MNNG) resulted in transformed NIH 3T3 foci. In vitro MNNG treatment of the plasmid, z-6, and transfection into NIH 3T3 cells led to the isolation of transformed cell lines. Screening of the in vitro and in vivo treated, transformed cell lines by RNA:RNA duplex mismatch analysis led to the detection of no mutations within the first exon of the human c-Ha-ras oncogene.

Thesis (MSc)--Stellenbosch University, 2002. / ENGLISH ABSTRACT: Please see fulltext for abstract / AFRIKAANSE OPSOMMING: Sien asb volteks vir opsomming

Thesis (MScMed)--Stellenbosch University, 2008. / ENGLISH ABSTRACT: In hypertrophic cardiomyopathy (HCM), an autosomal dominant disorder, hypertrophy is variable within and between families carrying the same causal mutation, suggesting a role for modifier genes. Associations between left ventricular hypertrophy and left ventricular pressure overload suggested that sequence variants in genes involved in the Renin-Angiotensin Aldosterone System (RAAS) may act as hypertrophy modifiers in HCM, but some of these studies may have been confounded by, amongst other things, lack of adjustment for hypertrophy covariates. To investigate this hypothesis, twenty one polymorphic loci spread across six genes (ACE1, AGT, AGTR1, CYP11B2, CMA and ACE2) of the RAAS were genotyped in 353 subjects from 22 South African HCM-families, in which founder mutations segregate. Genotypes were compared to 17 echocardiographically-derived hypertrophic indices of left ventricular wall thickness at 16 segments covering three longitudinal levels. Family-based association was performed by quantitative transmission disequilibrium testing (QTDT), and mixed effects models to analyse the X-linked gene ACE2, with concurrent adjustment for hypertrophy covariates (age, sex, systolic blood pressure (BP), diastolic BP, body surface area, heart rate and mutation status). Strong evidence of linkage in the absence of association was detected between polymorphisms at ACE1 and posterior and anterior wall thickness (PW and AW, respectively) at the papillary muscle level (pap) and apex level (apx). In single-locus analysis, statistically significant associations were generated between the CYP11B2 rs3097 polymorphism and PW at the mitral valve level (mit) and both PWpap and inferior wall thickness (IW)pap. Statistically significant associations were generated at three AGTR1 polymorphisms, namely, between rs2640539 and AWmit, rs 3772627 and anterior interventricular septum thickness at pap and rs5182 and both IWpap and AWapx. Furthermore, mixed effects model detected statistically significant association between the ACE2 rs879922 polymorphism and both posterior interventricular septum thickness and lateral wall thickness at mit in females only. These data indicate a role for RAAS gene variants, independent of hypertrophy covariates, in modifying the phenotypic expression of hypertrophy in HCM-affected individuals. / AFRIKAANSE OPSOMMING: Hipertrofiese kardiomiopatie (HCM), ‘n autosomale dominante afwyking, toon hoogs variërende hipertrofie binne en tussen families wat dieselfde siekte-veroorsakende mutasie het, hierdie dui op die moontlike betrokkenheid van geassosieerde modifiserende gene. Assosiasies tussen linker ventrikulêre hipertrofie en linker ventrikulêre druk-oorlading stel voor dat volgorde variasies in gene betrokke in die Renin-Angiotensin Aldosteroon Sisteem (RAAS) mag optree as hipertrofie modifiseerders in HCM. Sommige van hierdie soort studies is egter beperk omdat hulle nie gekompenseer het vir kovariante van hipertrofie nie. Om hierdie hipotese te ondersoek, is die genotipe bepaal by een-en-twintig polimorfiese lokusse, verspreid regoor ses RAAS gene (ACE1, AGT, AGTR1, CYP11B2, CMA and ACE2), in 353 kandidate vanuit 22 Suid-Afrikaanse HCM-families in wie stigter mutasies segregeer. Genotipes was vergelyk met 17 eggokardiografies afgeleide hipertrofiese indekse van linker ventrikulêre wanddikte by 16 segmente wat oor drie longitudinale vlakke strek. Familie-gebaseerde assosiasies was bestudeer deur kwantitatiewe transmissie disequilibrium toetsing (QTDT) en gemengde effek modelle om die X-gekoppelde geen ACE2 te analiseer, met gelyktydige kompensasie vir hipertrofie kovariate (ouderdom, geslag, sistoliese bloed druk (BP), diastoliese BP, liggaamsoppervlak area, hartritme en mutasie-status). Sterk indikasies van koppeling in die afwesigheid van assosiasie is waargeneem tussen ACE1 lokusse en posterior wanddikte (PW) asook anterior wanddikte (AW) by die papillêre spier vlak (pap) en die apeks vlak (apx). In enkel-lokus analises is statisties-betekenisvolle assosiasies gevind tussen die CYP11B2 rs3097 polimorfisme en PW by die mitraalklep vlak (mit) en beide die PWpap en inferior wanddikte (IW)pap. Statisties-betekenisvolle assosiasies was verder gevind by drie AGTR1 polimorfismes, naamlik, tussen rs2640539 polimorfisme en AWmit, rs3772627 en die anterior interventrikulêre septumdikte (aIVS) by die pap en rs5182 by beide die IWpap en AWapx. Gemengde-effek modelle het verder assosiasies aangetoon tussen die ACE2 rs879922 polimorfisme en die posterior interventrikulêre septumdikte en die laterale wanddikte by die mit, slegs in vrouens. Hierdie data dui op ‘n kovariaat-onafhanklike rol vir RAAS genetiese variante in die modifisering van die fenotipiese uitdrukking van hipertrofie in HCM-geaffekteerde individue.