Ascochyta blight (AB), caused by Ascochyta rabiei is a major disease of chickpea (Cicer arietinum L.), especially in areas where cool, cloudy, and humid weather persists during the crop season. Several epidemics of AB causing complete yield loss have been reported. The fungus mainly survives between seasons through infected seed and in infected crop debris. Despite extensive pathological and molecular studies, the nature and extent of pathogenic variability in A. rabiei have not been clearly established. Accumulation of phenols, phytoalexins (medicarpin and maackiain), and hydrolytic enzymes has been associated with host-plant resistance (HPR). Seed treatment and foliar application of fungicides are commonly recommended for AB management, but further information on biology and survival of A. rabiei is needed to devise more effective management strategies. Recent studies on inheritance of AB resistance indicate that several quantitative trait loci (QTLs) control resistance. In this paper we review the biology of A. rabiei, HPR, and management options, with an emphasis on future research priorities.

The causal agent of Ascochyta blight disease of chickpea (Cicer arietinum L.) is highly variable because of the presence of a sexual phase (Didymella rabiei). There is also selection pressure on the pathogen due to wide adoption of improved resistant chickpea cultivars in some countries. The pathogen is able to produce pathotypes with specific virulence on particular cultivars. Three pathotypes, I, II, and III, have been reported (3). In this study, we confirmed the presence of a new and highly virulent pathotype that we designate as pathotype IV. To test the pathogenicity of the isolates collected and maintained at ICARDA, 10 isolates representing a wide spectrum of pathogenic variation, including those classified by S. M. Udupa et al. (3) and a putatively identified more virulent type, which was collected from a chickpea production field in the Kaljebrine area, Syria, were inoculated onto a set of differential chickpea genotypes. The differential genotypes, ILC 1929, ILC 482, ILC 3279, and ICC 12004, were sown in individual 10-cm-diameter pots containing potting mix and arranged in a randomized block design with three replications in a plastic house maintained at 18 to 20°C. Each differential genotype was inoculated individually with the 10 isolates following the methodology of S. M. Udupa et al. (3). DNA was extracted from single-spored isolates to compare the genotypes of the isolates using three simple sequence repeat (SSR) markers (ArA03T, ArH05T, and ArH06T) (2) and to determine the frequency of mating types (MAT) through the use of MAT-specific PCR primers for MAT1-1 and MAT1-2 (1). Host genotype reactions were measured on a 1 to 9 rating scale (1 = resistant and 9 = plant death). On the basis of the pathogenicity tests, the isolates were classified into four pathotypes: I (least virulent, killed ILC 1929 but not ILC 482, ILC 3279, or ICC12004); II (virulent, killed ILC 1929 and ILC 482 but not ILC 3279 or ICC12004); III (more virulent, killed ILC 1929, ILC 482, and ILC 3279 but not ICC12004); and IV (highly virulent, killed all four host differentials). Of 10 single-spore isolates tested, four showed similar disease reactions unique to pathotype I, four revealed pathotype II reactions, and one isolate each behaved like pathotype III or pathotype IV. SSR fingerprinting of these isolates provided evidence for genetic diversity since SSR ArH05T was highly polymorphic and amplified five bands, including pathotypes III- and IV-specific bands, which need further investigation to discern if this locus has any role to play in the virulence. MAT-type analysis showed that seven isolates were MAT1-1 while the remaining three isolates were MAT1-2. Only pathotype I showed the profile of MAT1-2 and the other three pathotypes were MAT1-1. Initially, a number of chickpea wild relatives were screened to identify sources of resistance to pathotype IV, but none of the accessions tested showed resistance. However, efforts are underway to combine minor and major gene(s) available in the breeding program in addition to a further search of the wild gene pools to control pathotype IV. References: (1) M. P. Barve et al. Fungal Genet. Biol. 39:151, 2003. (2) J. Geistlinger et al. Mol. Ecol. 9:1939, 2000. (3) S.M. Udupa et al. Theor. Appl. Genet. 97:299, 1998.

Ascochyta blight induced by Ascochyta fabae f.sp . lentis is a major foliar disease affecting lentil . Screening 241 accessions of the ICARDA wild lentil germplasm collection for resistance to a Syrian isolate of this fungus was conducted under artificial inoculation in a plastic house . The reaction of resistant accessions was confirmed in a second trial . Twenty-four out of 16 accessions of Lens culinaris ssp . orientalis were resistant, as were 12 of 35 accessions of L . culinaris ssp . odemensis, 3 of 35 accessions of L . nigricans ssp . nigricans, 36 of 11 accessions of L . nigricans ssp . ervoides, and all 3 accessions of Vicia montbretii. Sixty-four per cent of resistant sources were from Syria and southeastern Turkey . Disease reaction was uncorrelated both to the altitude of collection and its annual average rainfall . A significant correlation (r = 0 .21 1) between leaflet width and disease reaction was due more to the frequency of the resistant reaction within the narrow-leaved L . nigricans ssp . ervoides than as a function of small leaf area. Disease reaction was uncorrelated with a range of other morphological traits .

Vascular wilt caused by Fusarium oxysporum f. sp. lentis Vasud. & Srin. is the major disease of the cultivated lentil (Lens culinaris Medikus). Host plant resistance is the most practical method of disease management. Wild lentils .represent an unexplored potential source for disease resistance and other characters. Screening 219 accessions of wild Lens Miller and 2 accessions of Vicia montbretii Fisch. & Mey. (syn. Lens montbretii (Fisch et Mey) Davis et Plitm.) for resistance to a Syrian isolate of this fungus at the seedling stage was conducted under artificial inoculation in a plastic house. Resistance at the reproductive growth stage was confirmed in pots in a plastic house and in a wilt-sick plot. Three accessions each of Lens culinaris ssp. orientatis (Boiss.) Ponert and L. nigricans M.B. Godr. ssp. nigricans Godr. and 2 ofL. nigricans ssp. ervoides (Brign.) Lad. maintained their resistance at the reproductive growth stage in the plastic house. All accessions of L. culinaris ssp. odemensis Lad. and V. montbretii were susceptible. However, in the sick-plot only three accessions (ILWL 79 & ILWL 113 of L. culinaris ssp. orientalis and ILWL 138 ofL. nigricans ssp. ervoides) maintained a good level of resistance. Resistance at the seedling stage was often found in accessions collected from northern and western sites of the distribution of the genus at low elevations. The most resistant accessions in the field at the reproductive growth stage were from Syria and Turkey.

The inheritance of resistance to lentil (Lens culinaris Medik.) vascular wilt caused by Fusarium oxysporum f.sp. lentis was investigated in a cross between resistant (ILL5588) and susceptible (L692–16‐l(s)) lines. F2:4 progenies and F6:8, F6:9 recombinant inbred line (RIL) populations were assessed for their wilt reaction for three seasons in a well‐established wilt‐sick plot. Resistance to wilt was conditioned by a single dominant gene in the populations studied. The map location of the Fw locus was identified for the first time through linkage to a random amplified polymorphic DNA (RAPD) marker (OPK‐15900) at 10.8 cM. Two other RAPD markers (OP‐BH800 and OP‐DI5500) identified by bulked segregant analysis were associated in the coupling phase with the resistance trait, and another marker (OP‐C04650) was associated with repulsion. The DNA markers reported here will provide a starting point in marker‐assisted selection for vascular wilt resistance in lentil.