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.

Novel species of fungi described in this study include those from various countries as follows: Australia, Chaetopsina eucalypti on Eucalyptus leaf litter, Colletotrichum cobbittiense from Cordyline stricta × C. australis hybrid, Cyanodermella banksiae on Banksia ericifolia subsp. macrantha, Discosia macrozamiae on Macrozamia miquelii, Elsinoë banksiigena on Banksia marginata, Elsinoë elaeocarpi on Elaeocarpus sp., Elsinoë leucopogonis on Leucopogon sp., Helminthosporium livistonae on Livistona australis, Idriellomyces eucalypti (incl. Idriellomyces gen. nov.) on Eucalyptus obliqua, Lareunionomyces eucalypti on Eucalyptus sp., Myrotheciomyces corymbiae (incl. Myrotheciomyces gen. nov., Myrotheciomycetaceae fam. nov.), Neolauriomyces eucalypti (incl. Neolauriomyces gen. nov., Neolauriomycetaceae fam. nov.) on Eucalyptus sp., Nullicamyces eucalypti (incl. Nullicamyces gen. nov.) on Eucalyptus leaf litter, Oidiodendron eucalypti on Eucalyptus maidenii, Paracladophialophora cyperacearum (incl. Paracladophialophoraceae fam. nov.) and Periconia cyperacearum on leaves of Cyperaceae, Porodiplodia livistonae (incl. Porodiplodia gen. nov., Porodiplodiaceae fam. nov.) on Livistona australis, Sporidesmium melaleucae (incl. Sporidesmiales ord. nov.) on Melaleuca sp., Teratosphaeria sieberi on Eucalyptus sieberi, Thecaphora australiensis in capsules of a variant of Oxalis exilis. Brazil, Aspergillus serratalhadensis from soil, Diaporthe pseudoinconspicua from Poincianella pyramidalis, Fomitiporella pertenuis on dead wood, Geastrum magnosporum on soil, Marquesius aquaticus (incl. Marquesius gen. nov.) from submerged decaying twig and leaves of unidentified plant, Mastigosporella pigmentata from leaves of Qualea parviflorae, Mucor souzae from soil, Mycocalia aquaphila on decaying wood from tidal detritus, Preussia citrullina as endophyte from leaves of Citrullus lanatus, Queiroziella brasiliensis (incl. Queiroziella gen. nov.) as epiphytic yeast on leaves of Portea leptantha, Quixadomyces cearensis (incl. Quixadomyces gen. nov.) on decaying bark, Xylophallus clavatus on rotten wood. Canada, Didymella cari on Carum carvi and Coriandrum sativum. Chile, Araucasphaeria foliorum (incl. Araucasphaeria gen. nov.) on Araucaria araucana, Aspergillus tumidus from soil, Lomentospora valparaisensis from soil. Colombia, Corynespora pseudocassiicola on Byrsonima sp., Eucalyptostroma eucalyptorum on Eucalyptus pellita, Neometulocladosporiella eucalypti (incl. Neometulocladosporiella gen. nov.) on Eucalyptus grandis × urophylla, Tracylla eucalypti (incl. Tracyllaceae fam. nov., Tracyllalales ord. nov.) on Eucalyptus urophylla. Cyprus, Gyromitra anthracobia (incl. Gyromitra subg. Pseudoverpa) on burned soil. Czech Republic, Lecanicillium restrictum from the surface of the wooden barrel, Lecanicillium testudineum from scales of Trachemys scripta elegans. Ecuador, Entoloma yanacolor and Saproamanita quitensis on soil. France, Lentithecium carbonneanum from submerged decorticated Populus branch. Hungary, Pleuromyces hungaricus (incl. Pleuromyces ge...

Lentil anthracnose (Colletotrichum truncatum (Schwein.) Andrus et W.D. Moore is a potential threat in many lentil (Lens culinaris Medik.) production regions of North America. In the lentil germplasm maintained in Germany and North America, 16 lines were reported to have resistance to race Ct1, but none has resistance reported to race Ct0. The objective of this study was to examine accessions of wild Lens species for their resistance to races Ct1 and Ct0 of lentil anthracnose. Five hundred and seventy-four wild accessions of six species and control lines were screened in two replications under both field and greenhouse conditions using a 1-9 scoring scale (1, highly resistant; 2-3, resistant; 4-5, moderately resistant; 6-7, susceptible; and 8-9, highly susceptible). Indianhead and PI 320937 were resistant while Eston and Pardina were susceptible to race Ct1 as expected. However, none of the check lines were resistant to race Ct0. Among the six Lens wild species tested, accessions of Lens ervoides (Brign.) Grande had the highest level of resistance, 3-5 to race Ct1 and Ct0 followed by L. lamottei Czefr. in the field and greenhouse. Lens orientalis (Boiss.), L. odemensis L., L. nigricans (M. Bieb.) Godron and L. tomentosus L. were highly susceptible, 8-9 to race Ct0 in the greenhouse. The highest frequency of resistance, especially in L. ervoides (Brign.) Grande, was found in accessions originating from Syria and Turkey. The usefulness of these L. ervoides (Brign.) Grande accessions as sources of resistance to the more virulent race of anthracnose in a lentil breeding program is discussed.

Lentil, Lens culinaris subsp. culinaris Medic., is an important legume crop on the Canadian prairies. Anthracnose, a fungal disease caused by Colletotrichum truncatum (Schwein.) Andrus & W.D. Moore, is a major barrier to seed yield and quality in lentil. Pathogenicity testing has revealed two races, Ct1 and Ct0, of C. truncatum in western Canada. No cultivar or landrace of cultivated lentil has been reported with resistance to anthracnose race Ct0. A search for Ct0 resistance in the wild species identified a high frequency of resistant accessions in Lens ervoides (Brign.) Grande. To incorporate higher levels of resistance from L. ervoides to the two races of anthracnose, a cross was made between a susceptible L. culinaris cultivar, Eston, and a resistant accession of L. ervoides germplasm, L‐01‐827A, which has both Ct0 and Ct1 resistance. Embryo rescue technique was used to obtain an F1 hybrid. Single‐seed descent was used to advance the individual F2 plants to F7:8 recombinant inbred lines. Evidence of transfer of resistance to both anthracnose races Ct1 and Ct0 from the wild species to cultivated lentil is presented. Chi‐square tests of goodness of fit indicated that resistance to race Ct1 and race Ct0 may be conferred by two recessive genes. However, these results may be skewed due to variable fertility encountered in development of the population. Selection of resistant lines for use in pyramiding genes in breeding programs should result in a more durable level of resistance to anthracnose in lentil.

Lens ervoides, a wild relative of lentil is an important source of allelic diversity for enhancing the genetic resistance of the cultivated species against economically important fungal diseases, such as anthracnose and Stemphylium blight caused by Colletotrichum lentis and Stemphylium botryosum, respectively. To unravel the genetic control underlying resistance to these fungal diseases, a recombinant inbred line (RIL) population (n = 94, F9) originating from a cross between two L. ervoides accessions, L01-827A and IG 72815, was genotyped on the Illumina HiSeq 2500 platform. A total of 289.07 million 100 bp paired-end reads were generated, giving an average 7.53-fold genomic coverage to the RILs and identifying 2,180 high-quality SNPs that assembled in 543 unique haplotypes. Seven linkage groups were resolved among haplotypes, equal to the haploid chromosome number in L. ervoides. The genetic map spanned a cumulative distance of 740.94 cM. Composite interval mapping revealed five QTLs with a significant association with resistance to C. lentis race 0, six QTLs for C. lentis race 1 resistance, and three QTLs for S. botryosum resistance. Taken together, the data obtained in the study reveal that the expression of resistance to fungal diseases in L. ervoides is a result of rearrangement of resistant alleles contributed by both parental accessions.

The hemibiotrophic fungus Colletotrichum truncatum causes anthracnose disease on lentils and a few other grain legumes. It shows initial symptomless intracellular growth, where colonized host cells remain viable (biotrophy), and then switches to necrotrophic growth, killing the colonized host plant tissues. Here, we report a novel effector gene, CtNUDIX, from C. truncatum that is exclusively expressed during the late biotrophic phase (before the switch to necrotrophy) and elicits a hypersensitive response (HR)-like cell death in tobacco leaves transiently expressing the effector. CtNUDIX homologs, which contain a signal peptide and a Nudix hydrolase domain, may be unique to hemibiotrophic fungal and fungus-like plant pathogens. CtNUDIX lacking a signal peptide or a Nudix motif failed to induce cell death in tobacco. Expression of CtNUDIX:eGFP in tobacco suggested that the fusion protein might act on the host cell plasma membrane. Overexpression of CtNUDIX in C. truncatum and the rice blast pathogen, Magnaporthe oryzae, resulted in incompatibility with the hosts lentil and barley, respectively, by causing an HR-like response in infected host cells associated with the biotrophic invasive hyphae. These results suggest that C. truncatum and possibly M. oryzae elicit cell death to signal the transition from biotrophy to necrotrophy.

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.

Cultivated lentil (Lens culinaris Medik. subsp. culinaris) has a relatively narrow genetic base and many commercial cultivars are susceptible to ascochyta blight caused by Ascochyta lentis Vassilievsky. A total of 375 accessions of six wild species of lentil received from ICARDA and 18 cultivated genotypes were screened for resistance to A. lentis under both field and greenhouse conditions in Saskatoon, Canada. A mixture of three monoconidial isolates of A. lentis was used as an inoculum and the level of infection rated using the Horsfall-Barratt scale (0-11). Accessions with resistance to A. lentis were observed in all wild species except for L. culinaris subsp. tomentosa (Ladiz.) Ferguson et al. showing no resistant accessions. Several consistently resistant accessions were found among entries of L. ervoides (Brign.) Grande and L. nigricans, (M. Bieb.) Godr., both of which belong to the secondary gene pool and a few in L. culinaris subsp. orientalis (Boiss.) Ponert and L. culinaris subsp. odemensis (Ladiz.) Ferguson et al. belonging to the primary gene pool. Some accessions of L. ervoides exhibited lower disease ratings and AUDPC values than the resistant control cv. 'Indianhead.' Thirteen accessions, previously reported as resistant to Syrian isolates of A. lentis were alsoresistant to the Canadian isolates; some also had resistance to anthracnose. The highest frequency of resistance was found in accessions of L. ervoides which originated from Syria and Turkey. These wild accessions represent a useful and untapped source for improving disease resistance in lentil.