Partial resistances, often controlled by quantitative trait loci (QTL), are considered to be more durable than monogenic resistances. Therefore, a precursor to developing efficient breeding programs for polygenic resistance to pathogens should be a greater understanding of genetic diversity and stability of resistance QTL in plants. In this study, we deciphered the diversity and stability of resistance QTL to Aphanomyces euteiches in pea towards pathogen variability, environments and scoring criteria, from two new sources of partial resistance (PI 180693 and 552), effective in French and USA infested fields. Two mapping populations of 178 recombinant inbred lines each, derived from crosses between 552 or PI 180693 (partially resistant) and Baccara (susceptible), were used to identify QTL for Aphanomyces root rot resistance in controlled and in multiple French and USA field conditions using several resistance criteria. We identified a total of 135 additive-effect QTL corresponding to 23 genomic regions and 13 significant epistatic interactions associated with partial resistance to A. euteiches in pea. Among the 23 additive-effect genomic regions identified, five were consistently detected, and showed highly stable effects towards A. euteiches strains, environments, resistance criteria, condition tests and RIL populations studied. These results confirm the complexity of inheritance of partial resistance to A. euteiches in pea and provide good bases for the choice of consistent QTL to use in marker-assisted selection schemes to increase current levels of resistance to A. euteiches in pea breeding programs.

Necrotrophic pathogens of the cool season food legumes (pea, lentil, chickpea, faba bean and lupin) cause wide spread disease and severe crop losses throughout the world. Environmental conditions play an important role in the development and spread of these diseases. Form of inoculum, inoculum concentration and physiological plant growth stage all affect the degree of infection and the amount of crop loss. Measures to control these diseases have relied on identification of resistant germplasm and development of resistant varieties through screening in the field and in controlled environments. Procedures for screening and scoring germplasm and breeding lines for resistance have lacked uniformity among the various programs worldwide. However, this review highlights the most consistent screening and scoring procedures that are simple to use and provide reliable results. Sources of resistance to the major necrotrophic fungi are summarized for each of the cool season food legumes. Marker-assisted selection is underway for Ascochyta blight of pea, lentil and chickpea, and Phomopsis blight of lupin. Other measures such as fungicidal control and cultural control are also reviewed. The emerging genomic information on the model legume, Medicago truncatula, which has various degrees of genetic synteny with the cool season food legumes, has promise for identification of closely linked markers for resistance genes and possibly for eventual map-based cloning of resistance genes. Durable resistance to the necrotrophic pathogens is a common goal of cool season food legume breeders.

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Asochyta blights of grain legumes are caused by fungal pathogens in the genus Ascochyta. Different species infect the different legume species, and in pea three species including Phoma medicaginis var. pinodella have been implicated in ascochyta blight. The impact of the diseases varies between crops, countries, seasons and cropping systems, and yield loss data collected under welldefined conditions is scarce. However, ascochyta blights are considered major diseases in many areas where legumes are grown. Symptoms appear on all aerial parts of the plant, and lesions are similar for most of the species, except for M. pinodes and P. medicaginis var. pinodella. Infected seed, stubble and/or air-borne ascospores are major sources of primary inoculum. Their importance varies between species and also between regions. All Ascochyta spp. produce rain-splashed conidia during the cropping season which are responsible for the spread of the disease within the crop canopy. Only in pea are ascospores involved in secondary disease spread. Limited data suggests that Ascochyta spp. may be hemibiotrophs; however, toxins characteristic for necrotrophs have been isolated from some of the species. Modelling of ascochyta blights is still in the developmental stage and implementation of such models for disease forecasting is the exception.

The pattern of development of pycnidia and perithecia of Mycosphaerella pinodes was studied in the glasshouse on pea plants (cv. Solara) sprayed with a pycnospore suspension and in field plots inoculated with barley grains colonized by the fungus. The numbers of pycnidia and perithecia were estimated on each stipule and internode of infected plants, and were related to ratings of disease severity (0-5 scale). Pycnidia were produced on both green and senescent organs, whereas perithecia only appeared on senescent organs. The development and quantity of pycnidia were related to initial inoculum concentration and the physiological stage of the plants. The formation of fruiting bodies progressed from the bottoms to the tops of plants during crop development. Spore trapping showed that both pycnospore dispersal and ascospore discharge were initiated by rainfall or dew. Pycnospores were principally trapped in the first 20 cm above the soil surface while ascospores were also trapped above the crop canopy. Pycnospores and ascospores were dispersed throughout the growing season, suggesting that ascospores also play an important role in secondary infections.

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The effects of temperature (5-30ЊC) and the duration of moisture on the development of ascochyta blight (Mycosphaerella pinodes) on pea seedlings, grown under controlled conditions, were investigated. The optimum temperature for monocyclic processes was 20ЊC. At this temperature, pycnidiospores germinated after 2 h, appressoria formed after 6 h and the germ-tube penetrated the leaf cuticle after 8 h. Disease symptoms were evident after 1 day of incubation and the first pycnidia formed after 3 days. Longer wetting periods were required for disease development and pycnidial formation at non-optimal temperatures. Disease severity and the number of pycnidia formed on leaves increased with temperature from 5 to 20ЊC, then decreased between 20 and 30ЊC. Polynomial equations were fitted to predict the stages of infection, incubation, latency and disease development as functions of temperature and duration of moisture. These equations allow comparisons of pathogen spread with plant development and could be incorporated into disease development models used for crop management programmes.

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