Doctor of Philosophy / Department of Agronomy / Allan K. Fritz / In this research, a recombinant inbred line (RIL) population derived from cross between a leaf rust- and stripe rust-susceptible spring wheat ‘Avocet S’ and a slow leaf- and stripe-rusting resistant spring wheat ‘Amadina’ was used to postulate and map leaf rust seedling resistance genes, identify quantitative trait loci (QTL) for slow-rusting resistance against leaf and stripe rust, and study slow leaf-rusting components, latent period and infection frequency. Two known Lr genes (Lr23, and Lr26) were identified to be present in ‘Amadina’ through gene postulation, pedigree, cytogenetic, and polymerase chain reaction analyses. One unknown gene associated with seedling resistance was also mapped on chromosome 1BL. In greenhouse experiment, it was estimated that at least five genes conditioning final disease severity (FS) and latent period (LP), and four genes conditioning infection frequency (IF), segregated in the population. Correlations between LP and FS, and LP and IF were moderately negative, and that between IF and FS was moderately positive, indicating inter-dependence of the traits. Two QTL on chromosomes 1BL and 6BL were associated with LP and FS, and three QTL on chromosomes 1BL, 6BL and 2DS were associated with IF. Segregation of the RIL population in field experiment indicated that there were at least four and three adult plant resistance (APR) genes involved in resistance for leaf and stripe rust. Six QTL on chromosomes 3AL, 4AL, 1BL, 5BL, and 7BL were associated with APR for leaf rust, and seven QTL on chromosome 4AL, 5AL, 1BL, 2BL, 4BL, 5BL, 2DL, and 4D were associated with APR for stripe rust. Our results indicated that the major portion of genetic variability for slow-rusting resistance was additive gene action, and, to some extent, epistasis. In this research, we also explored the utility of remote sensing and geographic information systems (GIS) and analytical operations to discriminate leaf rust pustules from other parts of leaf and to accurately determine pustule size in ‘Amadina’ and ‘Avocet S’.

Master of Science / Department of Plant Pathology / Erick D. DeWolf / Stripe rust, caused by Puccinia striiformis f. sp. tritici, historically has been a minor problem in the Great Plains. However, Kansas had significant losses due to stripe rust in 2001, 2003, and 2005. Recent research on the population of P. striiformis suggests changes in the fungal population may have been responsible for these epidemics. The objectives of this research were to determine conditions that are favorable for the infection of P. striiformis f. sp. tritici isolates from the current population and develop models to predict infection events. Two week old potted seedlings were inoculated with an isolate of P. striiformis and exposed to ambient weather conditions for 16 hours. Results of this bioassay were used to develop logistic regression models of infection. Models using hours at relative humidity >87%, leaf wetness, and mean relative humidity predicted infection with 93%, 80%, and 76% accuracy. Future research will use these results to determine weather patterns that influence the probability of stripe rust epidemics and to facilitate the development of regional prediction models for stripe rust. Foliar diseases of wheat result in an average yield loss of 7.8% in Kansas. Although it is possible to reduce these losses with foliar fungicides, the yield increases resulting from these applications may not justify the additional costs. The objective of this research was to develop models that help producers identify factors associated with disease-related yield loss and the profitable use of foliar fungicides. Data were collected for two years at three locations in central Kansas to determine yield response to fungicide application on eight varieties with varying degrees of resistance. Logistic regression was used to model the probability of a yield response >4 bushels per acre based on disease resistance of a variety, historical disease risk, and in-season disease risk. The accuracy of the resulting prediction models ranged from 84% to 71%. A model combining in-season disease risk and variety resistance was most accurate. The prediction accuracy of the model was 79% when tested with an independent validation dataset. In the future, these models will serve as educational tools to help producers maximize profit and productivity.

Doctor of Philosophy / Department of Agronomy / Guihua Bai / Guorong Zhang / Wheat yield and quality is influenced by many abiotic and biotic environmental factors. Pre-harvest sprouting (PHS) occurs when physiologically matured spikes are exposed to wet field conditions before harvest, which results in seed germination and causes significant losses in yield and end-use quality. Wheat stripe rust is one of the most important biotic factors reducing grain yield and quality. To investigate the genetic basis of the resistance to PHS and stripe rust in hard white winter wheat cultivars Danby and Tiger and develop molecular markers for marker- assisted breeding, a double haploid (DH) population, derived from those two cultivars, was genotyped with simple sequence repeats (SSR) markers and simple nucleotide polymorphism (SNP) markers. This DH population was assessed for resistance to PHS and stripe rust in both greenhouse and field experiments. For PHS, one major resistant quantitative trait locus (QTL) was consistently detected on the short arm of chromosome 3A in all three experiments conducted and explained 21.6% to 41.0% of the phenotypic variation (PVE). This QTL is corresponding to a previously cloned gene, TaPHS1. A SNP in the promoter of TaPHS1 co- segregated with PHS resistance in this mapping population. Meanwhile, two other QTLs, Qphs.hwwg-3B.1 and Qphs.hwwg-5A.1, were consistently detected on the chromosome arms 3BS and 5AL in two experiments. These two QTLs showed significant additive effects with TaPHS1 in improving PHS resistance. For stripe rust, three major QTLs were consistently detected in four out of six environments for infection type (IT) or disease severity (DS). Two of them, QYr.hwwg-2AS1 and QYr.hwwg-4BL1, contributed by the Danby allele explained up to 28.4% of PVE for IT and 60.5% of PVE for DS. The third QTL, QYr.hwwg-3BS1, contributed by the Tiger allele, had PVE values up to 14.7% for IT and 22.9% for DS. QYr.hwwg-2AS1 and QYr.hwwg- 4BL1 are likely the same resistance genes reported previously on chromosome arms 2AS and 4BL. However, QYr.hwwg-3BS1 might be different from the reported gene cluster near the distal end of 3BS where Yr57, Yr4, Yr30 and Sr2 were located. Significant additive effects on reducing IT and DS were observed among these three major QTLs. In order to pyramid multiple QTLs in breeding, user-friendly Kompetitive allele specific PCR (KASP) markers were successfully developed for several QTLs identified in this study. The QTLs and their interactions found in this study together with those novel flanking KASP markers developed will be useful not only for understanding genetic mechanisms of PHS and stripe rust resistance but also for marker- assisted breeding to improve wheat resistance to PHS and stripe rust by gene pyramiding.

Thesis (PhD (Agric)) -- Stellenbosch University, 2003. / ENGLISH ABSTRACT: Stripe (yellow) rust of wheat, caused by Puccinia striiformis f.sp. tritici, was first detected as a single introduction into South Africa in 1996. Two additional pathotypes have since been identified. Control of the disease may be achieved by use of genetic adult plant resistance (APR) as is present in the local cultivar 'Kariega'. The aim of this project was to understand the genetic basis of the APR in 'Kariega' to facilitate breeding of new varieties with genetic resistance to stripe rust. A partial linkage map of a 'Kariega X Avocet S' doubled haploid population covering all 21 wheat chromosomes was generated using 208 DNA markers, viz, 62 SSR, 133 AFLP, 3 RGA and 10 SRAP markers, and 4 alternative loci. The different marker techniques detected varying polymorphism, viz, overall SSR: 46%, AFLP: 7%, SRAP: 6% and RGA: 9%, and the markers produced low levels of missing data (4%) and segregation distortion (5%). A significant feature of the linkage map was the low polymorphism found in the D genome, viz, 19% of all mapped DNA markers, 11% of all AFLP markers and 30% of the total genome map distance. A region exhibiting significant segregation distortion was mapped to chromosome 4A and a seedling resistance gene for stem rust (Puccinia graminis f.sp . tritici), Sr26, mapped to chromosome 6A close to three SSR markers. The leaf tip necrosis gene, Ltn, which was also segregating in the population, mapped to chromosome 7D. Protocols for SRAP and RGA were optimised, and SRAP marker use in wheat genetic linkage studies is reported for the first time. The linkage map was used together with growth chamber and replicated field disease scores for QTL mapping. Chromosomes showing statistically significant QTL effects were then targeted with supplementary SSR markers for higher resolution mapping. The quality of disease resistance phenotypic data was confirmed by correlation analysis between the different scorers for reaction type (0.799±0.023) and for transformed percentage leaf area infected (0.942±0.007). Major QTL were consistently identified on chromosome 7D (explaining some 25-48% of the variation) and on chromosome 2B (21-46%) using transformed percentage leaf area infected and transformed reaction type scores (early and final) with interval mapping and modified interval mapping techniques. Both chromosomal regions have previously been identified in other studies and the 7D QTL is thought likely to be the previously mapped APR gene Yr 18. Minor QTL were identified on chromosomes lA and 4A with the QTL on 4A being more prominent at the early field scoring for both score types. A QTL evidently originating from 'Avocet S' was detected under growth chamber conditions but was not detected in the field, suggesting genotype-environment interaction and highlighting the need for modifications of growth chamber conditions to better simulate conditions in the field. The genetic basis of the APR to stripe rust exhibited by 'Kariega' was established by mapping of QTL controlling this trait. The linkage map constructed will be a valuable resource for future genetic studies and provides a facility for mapping other polymorphic traits in the parents of this population with a considerable saving in costs. / AFRIKAANSE OPSOMMING: Streep of geelroes van koring word veroorsaak deur Puccinia striiformis f. sp tritici, en is die eerste keer in 1996 in Suid-Afrika na introduksie van 'n enkele patotipe waargeneem. Twee verdere patotipes is sedertdien in Suid-Afrika gei"dentifiseer. Beheer van die siekte word veral moontlik gemaak deur die gebruik van genetiese volwasseplantweerstand soos gei"dentifiseer in die plaaslike kultivar 'Kariega'. Die doel van hierdie studie was om die genetiese grondslag van die streeproesweerstand te ontrafel ten einde die teling van nuwe bestande kultivars moontlik te maak. 'n Verdubbelde haplo1ede populasie uit die kruising 'Kariega X Avocet S' is aangewend om 'n gedeeltelike koppelingskaart vir die volle stel van 21 koring chromosome saam te stel. Die kaart het uit 208 DNA merkers, nl., 62 SSR, 133 AFLP, 3 RGA, 10 SRAP merkers en 4 ander lokusse bestaan. Totale polimorfisme wat deur die verskillende merkersisteme opgespoor is, was as volg: SSR: 46%, RGA: 9%, AFLP: 7% en SRAP: 6%. Die mate van ontbrekende data was gering (4%) asook die mate van segregasie distorsie (5%) van 'n enkele geval wat op chromosoom 4A gekarteer is. 'n Prominente kenmerk van die koppelingskaart is die relatiewe gebrek aan polimorfiese merkers op die D-genoom, nl., slegs 19% van alle DNA merkers en 11% van alle AFLP merkers wat slegs 30% van die totale genoom kaartafstand bestaan het. Die stamroes (Puccinia graminis f. sp. tritici) saailingweerstandsgeen, Sr26, karteer op chromosoom 6A naby drie SSR merkers. Die geen vir blaartipnekrose, Ltn, karteer op chromosoom 7D. Protokolle vir SRAP en RGA merkers is ge-optimiseer en gebruik van SRAP merkers in koppelings-analise word vir die eerste keer in koring gerapporteer. Die koppelingskaart is in kombinasie met groeikamerdata en gerepliseerde veldproefdata gebruik om die gene (QTL) vir volwasseplant streeproesweerstand te karteer. Chromosome met statisties betekenisvolle QTL is met aanvullende SSR merkers geteiken om die resolusie van kartering verder te verhoog. Die kwaliteit van fenotipiese data, soos in die proewe aangeteken, is bevestig deur korrelasies te bereken tussen lesings geneem deur onafhanklike plantpataloe (0.799 ± 0.023 vir reaksietipe en 0.942 ± 0.007 vir getransformeerde persentasie blaaroppervlakte besmet). Hoofeffek QTL vir die twee maatstawwe van weerstand is deur middel van die metodes van interval QTL kartering en gemodifiseerde interval QTL kartering konsekwent op chromosome 7D (25-48% van variasie verklaar) en 2B (21-46% van variasie verklaar) ge"identifiseer. In vorige studies is aangetoon dat beide chromosome 7D en 2B QTL vir volwasseplant streeproesweerstand dra. Die 7D QTL is waarskynlik die weerstandsgeen, Yr 18. QTL met klein effekte op weerstand is op chromosome lA en 4A ge"identifiseer. Die effek van laasgenoemde geen was meer prominent in die velddata in die vroee datum van weerstandsbeoordeling. Een QTL, afkomstig van 'Avocet S', is slegs onder groeikamertoestande identifiseerbaar. Dit dui op moontlike genotipe-omgewing wisselwerking en beklemtoon die noodsaaklikheid om aanpassings te maak in groeikamertoestande vir beter simulasie van veldproeftoestande. Die genetiese grondslag van volwasseplantweerstand teen streeproes in die kultivar 'Kariega' is deur QTL kartering bepaal. Die 'Kariega X Avocet S' koppelingskaart kan as 'n waardevolle basis dien vir toekomstige genetiese ontledings van ander polimorfiese kenmerke in die populasie.

L’adaptation des pathogènes à leurs hôtes et aux variations climatiques, particulièrement à la température est étudiée sur l’agent pathogène biotrophe obligatoire responsable de la rouille jaune du blé, Puccinia striiformis f. sp. tritici (Pst) au Moyen Orient. Cette étude s’est déroulée au Liban et en Syrie situés dans le berceau de la région de domestication du blé. Des gènes de résistance spécifique ont été postulés au stade plantule pour 87 lignées élites du programme d’amélioration de l’ICARDA,28 cultivars Libanais, et 23 landraces Libanaises en utilisant 11 pathotypes français disponibles à l’INRA-BIOGER. Un seul gène et une combinaison de gènes ont été postulés dans les lignées elites. Neuf gènes de résistance ont été identifiés dans les lignées élites ; plus de génotypes résistants figuraient parmi les lignées issues du programme d’amélioration. Les landraces sont les plus sensibles mais ont montré une ségrégation de réaction résistance parmi les plants sensibles.Pour la structuration de population pathogène du Liban et de la Syrie, un échantillonnage a été fait dans les deux pays sur du blé tendre, du blé dur et des repousses durant 2010-2011. Six isolats Libanais et 48 isolats Syriens ont été pathotypés avec une gamme de 43 hôtes différentiels. 275 échantillons ont été génotypés avec 20 marqueurs SSR. La population était clonale malgré avec la présence de l’hôte secondaire Berberis sp. dans la région, toutefois un nombre élevé de 50 MLG est observé était pour une population clonale. La présence de la race invasive PstS1/PstS2 caractérise cette région. Le profil de virulence Vr2, 6, 7, 9, 27 est le plus fréquent et typique du groupe génétique Méditerranéen (Bahri et al., 2009). La virulence Vr8 n’est pas fixée dans la population malgré sa présence dans la race invasive décrite depuis l’an 2000 (Milus et al., 2009). L’adaptation de la rouille jaune à la température a été décrite par Milus et al. (2009) et Mboup et al. (2012). Notre étude d’adaptation à la température a été faite sur un échantillon de 26 isolats provenant de zones froides et chaudes avec 4 isolats de référence. Nous avons testé deux paramètres d’agressivité, efficacité d’infection et période de latence sous quatre différents régimes de température (Chaud versus froid pour période de rosée et période d’incubation). Les isolats diffèrent pour leur réponse aux variations de température. Quelques isolats montrent une efficacité d’infection et une courte période de latence sous les différents régimes, d’autres sont efficaces au froid mais pas au chaud et vice versa. Pour l’efficacité d’infection, il n’y a pas d’adaptation mais par contre pour la période de latence on montre une adaptation à la température des isolats de la zone chaude ayant une efficacité d’infection. La température chaude de rosée a retardé la période de latence mais ce phénomène a été moins marqué pour les isolats d’origine chaude quand c’est incubé au chaud. Cette étude a montré que la population est clonale avec un haut nombre de pathotypes. Le germplasme n’est pas diversifié avec des gènes de résistance contre la rouille jaune. L’adaptation de l’agent de la rouille jaune à la température parmi les isolats testés a été décrite pour la période de latence pour les isolats provenant d’origine chaude. / The adaptation of fungal pathogen to its hosts and to the climate variation, in particular to the temperature, was investigated on wheat stripe (yellow) rust, caused by the biotroph fungus Puccinia striiformis f. sp. tritici (Pst) in the Middle East, focusing on Lebanon and Syria. This disease is a major problem for the crop in the region. Specific resistance genes were postulated in 138 wheat genotypes including elite lines, grown varieties and local landraces, using an array of 11 French pathotypes. Resistance gene diversity for yellow rust in wheat elite lines was higher than in current, commercial varieties grown in Lebanon, with nine Yr genes detected singly or in combination. Some varieties were resistant to all tested pathotypes and might provide interesting sources of resistance. Most of the Lebanese landraces were susceptible but also heterogeneous by their number of plants susceptible and resistant to a specific pathotype in a same landrace.A field survey was conducted in Lebanon and Syria in 2010-2011 and 275 Pst isolates were collected. The pathogen population was genotyped with 20 microsatellite markers and was found to be clonal, although the alternate host Berberis libanotica is present in the region. The dominant multilocus genotype shared similarity with the new invasive strain PstS1/PstS2 dispersed worldwide since 2000. The population was clonal with 10 pathotypes detected in Lebanon and Syria. 50 MLGs were detected considered high for clonal population. The virulence profiles combining Vr2, Vr6, Vr7, Vr9, and Vr27 are typical of the Mediterranean area according to group (Bahri et al., 2009) and corresponded to the worldwide invasive pathotype described since 2000 (Milus et al., 2009). The Vr8 was not fixed in this population, whereas this virulence is frequent in the Mediterranean genetic group (Bahri et al., 2009).Recently Pst strains have been described for adaptation to warm temperature (Milus et al., 2009; Mboup et al., 2012). The question of temperature adaptation in this study was whether the strains adapted to warm temperature are found in few clones of invasive strains or if they are selected in different pathogen genotypes locally under specific climate conditions. We selected 26 Pst isolates from the Middle East, 13 isolates from warm and 13 isolates from cold areas. We assessed their infection efficiency and latent period under four temperature regimes (high and warm temperature for the spore penetration phase, and high and warm temperature for the latency period). The isolates differed for the thermal aptitude for infection efficiency and latent period, but no clear relationship was established between the climate of the origin location of the isolate and its thermal aptitude. Some isolates were able to infect at high temperature but had long latency at high temperature and vice versa, some isolates had low infection efficiency and short latent period at high temperature, and few isolates were efficient either at high temperature or cold temperature for infection efficiency. Latency period showed pattern of local adaptation. Warm dew temperatures retarded sporulation, but this effect was far less marked for isolates from warm climates when incubated under warm conditions.This study provides details about probable effective yellow rust genes present in different genotypes and the prevalent pathotypes in the region. Moreover, the thermal aptitude for infection efficiency and latent period of some isolates under contrasting temperature will help us to build a better integrated disease management in the highlight of global warming.

Disease resistance is critical in soft red winter wheat (Triticum aestivum L.) cultivars. Leaf rust caused by Puccinia triticina Eriks and stripe rust caused by Puccinia striiformis Westend. f.sp. tritici Eriks. are destructive pathogens of wheat. From 2014 to 2015 phenotypic data was collected at diverse locations for resistance to leaf rust (North Carolina, Texas, and Virginia) and stripe rust (Arkansas, North Carolina, Georgia, Texas, and Virginia) in a Pioneer ‘25R47’ /‘Jamestown’ (P47/JT) population composed of 186 F5:9 recombinant inbred lines (RILs). Analysis of the P47/JT population identified two quantitative trait loci (QTL) for leaf rust resistance on chromosome 5B and two QTL for stripe rust resistance on chromosomes 3B and 6A. Phenotypic variation (%) explained by the putative leaf rust resistance QTL of Jamestown on 5B was as high as 22.1%. Variation explained by the putative stripe rust resistance QTL of Jamestown on 3B and 6A was as high as 11.1 and 14.3%, respectively. Jamestown is postulated to contain gene Lr18. Seedlings of 186 F5:9 recombinant inbred lines from the P47/JT population and 200 F2 seedlings from eight other crosses including Jamestown and/or the Lr18 host differential line RL6009 (Thatcher*6/Africa 43) were screened with P. triticina race TNRJJ. Genetic analysis of the populations was conducted to validate the presence of Lr18 in Jamestown. Results of linkage analysis identified SNP maker IWB41960 linked within 5 cM of gene Lr18 in all three populations. From 2016 to 2017 phenotypic data was collected at diverse locations for resistance to leaf rust (Illinois, North Carolina, and Virginia) in a ‘2013412’ (PI 667644) / VA10W-21 (PI 676295) population (412/21) composed of 157 doubled haploid (DH) lines. The 412/21 DH lines were genotyped via genotyping by sequence (GBS). Analysis of the 412/21 population identified one quantitative trait loci (QTL) region associated with adult plant resistance to leaf rust on chromosome 1B. Phenotypic variation (%) explained by the putative leaf rust resistance QTL of 2013412 on 1B was as high as 40.1%. Kompetitive allele-specific (KASP) markers KASP_S1B_8414614 and KASP_S1B_8566239 were developed as markers for use in marker assisted selection. / Ph. D. / Disease resistance to leaf rust and stripe rust is important when growing soft red winter wheat. Genetic resistance can have a benefit to cost ratio of up to 27:1, considerably better than that of fungicide treatments. From 2013 to 2017 disease data was collected across multiple locations spanning the eastern United States (Arkansas, Georgia, Illinois, North Carolina, Texas, and Virginia). DNA molecular markers were used to identify specific chromosome regions containing genes associated with leaf and stripe rust resistance. DNA markers associated with genes conferring resistance to leaf rust resistance were identified in three chromosome regions, and genes in two regions were associated with stripe rust resistance. These genes and molecular markers associated with them can be used by scientists to further enhance resistance in wheat cultivars. Another study was conducted to determine if Lr18, a gene for leaf rust resistance that has a large effect, is present in the Virginia Tech soft red winter wheat breeding material. This gene (Lr18) is known to have been introduced from an ancestral species highly related to wheat. Wheat seedlings derived from crosses between lines postulated to carry Lr18 with susceptible lines were tested for resistance to a specific strain of leaf rust lacking virulence to Lr18. Genetic analysis of the ratio of resistant versus susceptible seedlings and association between DNA molecular markers and resistant seedlings were conducted to validate the presence of gene Lr18. A molecular marker linked tightly to gene Lr18 was identified in the study. This gene was found to be widely distributed in soft red winter wheat breeding materials and the molecular marker associated with gene Lr18 will be useful for scientists to further improve resistance in wheat cultivars.

Leaf rust and stripe rust of wheat (Triticum aestivum L.) are caused by the fungal pathogens Puccinia triticina, and Puccinia striiformis f.sp. tritici, respectively. In North America, the incorporation of adult-plant resistance (APR) genes into breeding lines has been an important strategy to achieve durable resistance to both diseases. Previously, the spring wheat cultivar AC Domain was reported to express an effective level of adult-plant resistance (APR) to leaf rust under field conditions. Early gene postulation work had suggested AC Domain might carry the APR gene Lr34 due to its phenotypic similarity to other Lr34 carrying lines. However, new gene specific markers have shown that AC Domain is not a carrier of Lr34. The objective of this research was to genetically localize the resistance in AC Domain, which is important because the cultivar has frequently been used as a parent in Canadian breeding programs, primarily for its value as a source of pre-harvest sprouting resistance. A mapping population of 185 doubled haploid (DH) lines derived from the cross ‘RL4452’ by ‘AC Domain’ was used for this study. RL4452 is a known carrier of Lr34. During 2011-2012, the DH population was evaluated in field leaf rust nurseries at Saskatoon, SK and Portage, MB and at a stripe rust nursery at Lethbridge, AB. Field results indicated that rust resistance in the mapping population was variable, with lines ranging from highly resistant, to highly susceptible. DH lines carrying Lr34 showed a high level of resistance to both diseases. Thus, the non-Lr34 carriers were genotyped using select SSR markers, and by an Illumina 9k Infinium iSelect SNP assay for subsequent quantitative trait loci (QTL) analysis. QTL analysis revealed that AC Domain donated a major resistance QTL located on chromosome 2BS, that mapped 46 cM proximal to markers linked to Lr16, and explained a significant portion of the leaf and stripe rust phenotypic variance in all test environments. In addition, this QTL was significantly associated with the expression leaf tip necrosis (LTN), reduction in area under the disease progress curve (AUDPC), and coefficient of infection (CI). In certain environments the interaction between the 2B QTL and Lr34 was additive resulting in a superior level of rust resistance. Indoor rust testing showed AC Domain was susceptible to both diseases at the seedling stage. Taken together these results suggest that the identified resistance in AC Domain is likely due to the presence of an APR gene, on chromosome 2BS.

Studies were conducted on three field trials of wheat cv. Kopara to investigate the lack of compensation by later determined components of yield because of early disease constraints. The investigation was based on the hypothesis that early disease reduces root development and thus causes the plants to be water constrained at later growth stages when soil water deficits usually occur. The reduced root development and soil water deficits may reduce the ability of the plant to compensate for reductions in early determined components. The hypothesis was tested by the application of irrigation to alleviate water stress. In a disease free crop, the possible phytotonic effects of the fungicides benomyl and triadimefon on wheat were investigated. These fungicides had no phytotonic effects on shoot, root growth, or yield under the prevailing conditions. The effect of disease on root development was analysed by root length measurements. Disease present in the crop at any stage of growth affected root development. Root development in the upper zones of the soil profile was reduced more by disease compared to those zones below 35 cm. A full disease epidemic reduced root development more than an early or late disease epidemic. The early and late disease epidemics had similar effects on root length. Alleviation of early disease constraints enabled greater development of roots to offset any earlier reductions. Soil water deficits increased root development in the lower zones of the nil disease plants. The presence of adequate soil water from irrigation reduced the requirement for further root growth in all treatments. In the 1981-1982 field trial a full disease epidemic reduced yield by 14% whereas an early disease epidemic reduced yield by 7%. The reduction in yield was attributed to a lower grain number. With irrigation the yield reduction in the full disease plants was 12% whereas in the early disease plants the reduction was only 2.4%. This indicated that plants affected by the early disease epidemic were water constrained. In this study, the results suggested that, for conditions prevailing in Canterbury, the supply of water at later growth stages increased grain weight in plants which were subject to early disease epidemics. This suggests that reduced root development caused by early disease and soil water deficits may prevent compensation by grain weight. Water use was similar in all disease treatments. After irrigation the irrigated plants of all treatments used more water. Disease affected water use in relation to yield production however, and was better expressed by water use efficiency. Water use efficiency was reduced in the full disease plants. A stepwise regression analysis suggested that water use efficiency was affected directly by disease at later growth stages, and indirectly via an effect on total green leaf area at early growth stages. This study partially proves the hypothesis that reductions in root development caused by an early disease epidemic may constrain the plants at later growth stages when water deficits usually occur. It was shown that the reduction in root development caused by disease could be counteracted by irrigation. In this respect, water served as a tool to study the effect of disease constraints on the yield of wheat. A knowledge of cereal crop physiology, root growth and function is used to explain and discuss the observations made in this research programme. The results are discussed in relation to the way in which disease affects yield through its effect on root development. The possible reasons for the continued effects of disease even after the control of disease at later growth stages are discussed. The economic use of fungicides and water in diseased crops are also outlined. Suggestions for future studies on disease-yield loss relationships are provided. The repetition of these experiments in different sites and climatic regions could provide information which may be incorporated in disease-yield loss simulation models. This could then be used to predict root development and water requirements of diseased plants, and provide a basis for economic use of fungicides and water, and for better disease management programmes.