The importance of various factors influencing the evolution of herbicide resistance in weeds is critically examined using population genetic models. The factors include gene mutation, initial frequency of resistance alleles, inheritance, weed fitness in the presence and absence of herbicide, mating system, and gene flow. Where weed infestations are heavy, the probability of selecting for resistance can be high even when the rate of mutation is low. Subsequent to the occurrence of a resistant mutant, repeated treatments with herbicides having the same mode of action can lead to the rapid evolution of a predominantly resistant population. At a given herbicide selection intensity, the initial frequency of resistance alleles determines the number of generations required to reach a specific frequency of resistant plants. The initial frequency of resistance alleles has a greater influence on the evolutionary process when herbicides impose weak selection, as opposed to very strong selection. Under selection, dominant resistance alleles increase in frequency more rapidly than recessive alleles in random mating or highly outcrossing weed populations. In highly self-fertilizing species, dominant and recessive resistance alleles increase in frequency at approximately the same rate. Gene flow through pollen or seed movement from resistant weed populations can provide a source of resistance alleles in previously susceptible populations. Because rates of gene flow are generally higher than rates of mutation, the time required to reach a high level of resistance in such situations is greatly reduced. Contrary to common misconception, gene flow from a susceptible population to a population undergoing resistance evolution is unlikely to slow the evolutionary process significantly. Accurate measurements of many factors that influence resistance evolution are difficult, if not impossible, to obtain experimentally. Thus, the use of models to predict times to resistance in specific situations is markedly limited. However, with appropriate assumptions, they can be invaluable in assessing the relative effectiveness of various management practices to avoid, or delay, the occurrence of herbicide resistance in weed populations.

A major fusarium head blight (FHB) resistance gene Fhb1 (syn. Qfhs.ndsu-3BS) was fine mapped on the distal segment of chromosome 3BS of spring wheat (Triticum aestivum L.) as a Mendelian factor. FHB resistant parents, Sumai 3 and Nyubai, were used as sources of this gene. Two mapping populations were developed to facilitate segregation of Qfhs.ndsu-3BS in either a fixed resistant (Sumai 3*5/Thatcher) (S/T) or fixed susceptible (HC374/3*98B69-L47) (HC/98) genetic background (HC374 = Wuhan1/Nyubai) for Type II resistance. Type II resistance (disease spread within the spike) was phenotyped in the greenhouse using single floret injections with a mixture of macro-conidia of three virulent strains of Fusarium graminearum. Due to the limited heterogeneity in the genetic background of the crosses and based on the spread of infection, fixed recombinants in the interval between molecular markers XGWM533 and XGWM493 on 3BS could be assigned to discrete "resistant" and "susceptible" classes. The phenotypic distribution was bimodal with progeny clearly resembling either the resistant or susceptible parent. Marker order for the two maps was identical with the exception of marker STS-3BS 142, which was not polymorphic in the HC/98 population. The major gene Fhb1 was successfully fine mapped on chromosome 3BS in the same location in the two populations within a 1.27-cM interval (S/T) and a 6.05-cM interval (HC/98). Fine mapping of Fhb1 in wheat provides tightly linked markers that can reduce linkage drag associated with marker-assisted selection of Fhb1 and assist in the isolation, sequencing and functional identification of the underlying resistance gene.

Fusarium head blight (FHB) is one of the most important fungal wheat diseases worldwide. Understanding the genetics of FHB resistance is key to facilitate the introgression of different FHB resistance genes into adapted wheat. The objective of this project was to study the FHB resistance QTL on chromosome 6B, quantify the phenotypic variation, and qualitatively map the resistance gene as a Mendelian factor. The FHB resistant parent BW278 (AC Domain*2/Sumai 3) was used as the source of the resistance allele. A large recombinant inbred line (RIL) mapping population was developed from the cross BW278/AC Foremost. The population segregated for three known FHB resistance QTL located on chromosomes 3BSc, 5A, and 6B. Molecular markers on chromosome 6B (WMC104, WMC397, GWM219), 5A (GWM154, GWM304, WMC415), and 3BS (WMC78, GWM566, WMC527) were amplified on approximately 1,440 F2:7 RILs. The marker information was used to select 89 RILs that were fixed homozygous susceptible for the 3BSc and 5A FHB QTLs and were recombinant in the 6B interval. Disease response was evaluated on 89 RILs and parental checks in the greenhouse and field nurseries. Dual floret injection (DFI) was used in greenhouse trials to evaluate disease severity (DS). Macroconidial spray inoculations were used in field nurseries conducted at two locations in southern Manitoba (Carman and Glenlea) over two years 2003 and 2004, to evaluate disease incidence, disease severity, visual rating index, and Fusarium-damaged kernels. The phenotypic distribution for all five-disease infection measurements was bimodal, with lines resembling either the resistant or susceptible checks and parents. All of the four field traits for FHB resistance mapped qualitatively to a coincident position on chromosome 6BS, flanked by GWM133 and GWM644, and is named Fhb2. The greenhouse-DS trait mapped 2 cM distal to Fhb2. Qualitative mapping of Fhb2 in wheat provides tightly linked markers that can reduce linkage drag associated with marker assisted selection of Fhb2 and aid the pyramiding of different resistance loci for wheat improvement.

An F1 derived doubled haploid (DH) population of 402 lines from the adapted spring wheat cross Superb (high yielding)/BW278 (low yielding) was developed to identify quantitative trait loci (QTL) associated with yield and yield components. A subset of the population (186 lines) was evaluated in replicated field trials in 2001 and 2002 at six locations in Manitoba and Saskatchewan, Canada. Agronomic parameters, grain yield and yield components including 1,000 grain weight, harvest index, average seed weight spike(-1), seed number spike(-1) and spikes number m(-2) were measured. A genetic map was constructed with 268 microsatellite marker loci and included two morphological genes, reduced plant height, Rht-B1b, and the presence/absence of awns, B1. Composite interval mapping was conducted to estimate the location and effect of QTL associated with the evaluated traits. A total of 53 QTL were identified on 12 chromosomes for the 9 evaluated traits with the coefficient of determination ranging from 0.03 to 0.21 of the total variation. The increase in yield and yield components ranged from 4.5 to 17.1% over the population mean. The five grain yield QTL were detected on chromosomes 1A, 2D, 3B, and 5A and showed a combined increase of 34.4%, over the population mean. The alleles from Superb were associated with increased yield for four of the five QTL. This study identified potential chromosome segments for use in marker-assisted selection to improve yield and yield components in spring wheat.

The inheritance of resistance to dicamba in wild mustard was determined by making reciprocal crosses between a resistant (R) population derived from a field treated repeatedly with auxin-type herbicides, and a known susceptible (S) population. The resulting F1 hybrids were selfed to produce F2 populations and backcrossed to the S parent. At the three- to four-leaf stage, parental, F1, F2, and backcross populations were screened for resistance to dicamba at three dosages (50, 200, and 400 g ai ha−1). F1 progeny survived all dosages and exhibited levels of injury similar to the R parental population. F2 populations segregated in a 3:1 ratio of R to S phenotypes. Progeny of backcrosses segregated in a 1:1 (R:S) ratio. Responses of the F1, F2, and backcross populations to treatment with dicamba indicate that resistance is determined by a single, completely dominant nuclear allele.

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Hard white wheat (Triticum aestivum L.) is a value-added product because of its processing advantages over red wheat; however, white wheat tends to be more susceptible to pre-harvest sprouting (PHS). To identify quantitative trait loci (QTLs) associated with PHS tolerance, we developed a doubled haploid (DH) mapping population from the cross AC Domain (red seeded) 9 White-RL4137 (white seeded). A genetic map was constructed using microsatellite markers located on chromosome groups 3, 4, 5 and 6. A population of 174 DH lines was characterized for important aspects of PHS including sprouting index, germination index, Hagberg falling number and seed coat colour. A total of 11 QTLs were identified on group 3 chromosomes and on chromosome 5D. Seven QTLs associated with the PHS traits were found to be co-incident with seed coat colour on chromosomes 3A, 3B and 3D. The 5D PHS QTL was notable because it is independent of seed coat colour.

A high level of cold hardiness is essential to ensure consistent overwintering of wheat (Triticum aestlvum L.) in the Northern Great Plains region of North America. Consequently, a clear understanding of the genetic control of cold hardiness would facilitate plant breeding efforts directed at cultivar improvement for this area. Although several genetic studies have been conducted, there is not a general consensus on the mode of gene action controlling the expression of cold hardiness in wheat. This study used one spring and four winter cultivars representing a wide range of cold hardiness potential to investigate the mode of inheritance and interaction of cold hardiness, determined in a controlled environment that allowed for maximum expression of cold hardiness potential, and vernalization requirement in wheat. Differences in growth habit between parental cultivars were controlled by the Vrn~ gene. Cold hardiness, estimated as the temperature at which 50% of the plant population was killed (LT5o), was controlled by genes with either dominant or additive effects. At least one dominant gene was associated with cold hardiness differences between spring and winter wheat, while genes with mainly additive effects determined differences in cold hardiness among cultivars with the winter growth habit. Broad sense heritability estimates for LT5o in the controlled environment considered ranged from 0 to 88% with most estimates exceeding 50%. In the F2-derived F 3 generation, hardy transgressive segregates were most common in crosses between relatively nonhardy cultivars, but no segregates were significantly hardier than the hardiest parental cultivar. Lack of a vernalization requirement did not hinder the development of cold hardiness; however, distribution of F2-derived F 3 lines provided evidence of possible genetic linkage or pleiotropism between the gene segregating for growth habit and a gene or genes controlling cold hardiness. C OLD HARDINESS iS a complex quantitative trait conditioned by the plant genotype and the environment in which the plant is grown (Rohde and Pulham, 1960). Although several genetic studies have