Ascochyta blight, caused by Ascochyta rabiei (Pass.) Lab., is a devastating disease of chickpea (Cicer arietinum L.) worldwide. Resistant germplasm has been identified and the genetics of resistance has been the subject of numerous studies. The objectives of the present study were to determine the genetics of resistance to ascochyta blight of chickpea and to map and tag the chromosomal regions involved using molecular markers. We used a set of 142 F5:6 recombinant inbred lines (RILs) obtained from an interspecific cross of C. arietinum (FLIP84‐92C, resistant parent) × C. reticulatum Lad. (PI 599072, susceptible parent). The RILs were scored for disease reactions in the field over 2 yr and were genotyped for polymorphic molecular markers [isozyme, random amplified polymorphic DNA (RAPD), and inter simple sequence repeat (ISSR)] in the laboratory. The disease was scored quantitatively and data were used for QTL analysis. A linkage map was established that comprised nine linkage groups containing 116 markers covering a map distance of 981.6 centimorgans (cM) with an average distance of 8.4 cM between markers. Two quantitative trait loci (QTLs), QTL‐1 and QTL‐2, conferring resistance to ascochyta blight, were identified which accounted for 50.3 and 45.0% of the estimated phenotypic variation in 1997 and 1998, respectively, and were mapped to linkage groups 6 and 1, respectively. Two RAPD markers flanked QTL‐1 and were 10.9 cM apart while one ISSR marker and an isozyme marker flanked QTL‐2 and were 5.9 cM apart. These markers can be used for marker‐assisted selection for ascochyta blight resistance in chickpea breeding programs, and to develop durable resistant cultivars through gene pyramiding.

The combination of several self-reported items may be useful for ascertainment of periodontal disease in epidemiologic studies.

Perennial ryegrass (Lolium perenne L.) is an outcrossing, wind-pollinated species exhibiting a gametophytic two-locus system of self-incompatibility (S and Z). The two incompatibility loci were genotyped in a cross between a doubled-haploid plant crossed as the female parent with a normal heterozygous plant. The S and Z loci were found to segregate in the expected 1:1 ratio and also segregated independently. The two loci were mapped to linkage groups one and two respectively, in accordance with the Triticeae consensus map. In addition, there were notable associations

The historical and contemporary population genetic structure of the chickpea Ascochyta blight pathogen, Ascochyta rabiei (teleomorph: Didymella rabiei), was determined in the US Pacific Northwest (PNW) using 17 putative AFLP loci, four genetically characterized, sequence-tagged microsatellite loci (STMS) and the mating type locus (MAT). A single multilocus genotype of A. rabiei (MAT1-1) was detected in 1983, which represented the first recorded appearance of Ascochyta blight of chickpea in the PNW. During the following year many additional alleles, including the other mating type allele (MAT1-2), were detected. By 1987, all alleles currently found in the PNW had been introduced. Highly significant genetic differentiation was detected among contemporary subpopulations from different hosts and geographical locations indicating restricted gene flow and/or genetic drift occurring within and among subpopulations and possible selection by host cultivar. Two distinct populations were inferred with high posterior probability which correlated to host of origin and date of sample using Bayesian model-based population structure analyses of multilocus genotypes. Allele frequencies, genotype distributions and population assignment probabilities were significantly different between the historical and contemporary samples of isolates and between isolates sampled from a resistance screening nursery and those sampled from commercial chickpea fields. A random mating model could not be rejected in any subpopulation, indicating the importance of the sexual stage of the fungus both as a source of primary inoculum for Ascochyta blight epidemics and potentially adaptive genotypic diversity.

Fusarium wilt caused by Fusarium oxysporum Schlechtend.:Fr. f. sp. ciceris (Padwick) Matuo & K. Sato is the most widely spread soilborne disease of chickpea (Cicer arietinum L.). To advance our understanding of the genetics of wilt resistance and aid chickpea breeding programs, we developed a set of F6 recombinant inbred lines (RILs) between Fusarium wilt susceptible (C‐104) and resistant 315) parents. Prior screening of selected F3 plants identified two primers (UBC‐170 and CS‐27) that produced random amplified polymorphic DNA {RAPD) markers associated with Fusarium wilt race 1 resistance. Analysis of the RILs with these primers yielded an estimate of 7% recombination between the two markers and the locus for wilt resistance, and 6% recombination between the loci corresponding to the two RAPD markers. The DNA fragments were cloned and sequenced in order to construct primers that would amplify only the markers of interest. Primer pair CS‐27F/CS‐27R amplified a fragment linked to the allele for susceptibility to race 1 of Fusarium wilt and thus constitute allele specific associated primers (ASAPs), whereas UBC‐170FFLIBC‐170R produced a single band for both resistant and susceptible genotypes, thus demonstrating locus specificity rather than allele specificity. The use of markers generated by the RAPD or ASAP approaches can facilitate the introgression of resistance genes into susceptible lines and expedite the screening of chickpea germplasm resources and will be useful in extending the genetic map of chickpea.

Ascochyta blight (caused by Ascochyta rabiei [Pass] Labr.) is a devastating and widespread disease of chickpea (Cicer arietinum L.). Studies of the genetics of resistance to blight have generated inconsistent reports due to year to year and between location variation in screening trial results. Most previous studies have relied on F2 or backcross populations for segregation analyses; however, inheritance patterns have been difficult to confirm because of the inability to repeat the evaluations in time and space. The objective of this study was to determine the inheritance of resistance to ascochyta blight in chickpea using recombinant inbred line (RIL) populations. The RILs were derived from two intraspecific crosses, PI 359075(1) × FLIP 84‐92C(2), ‘Blanco Lechoso’ × ‘Dwelley’, and one interspecific cross, FLIP 84‐92C(3) × C. reticulatum Lad. (PI 599072). The resistant parents, FLIP 84‐92C and Dwelley, had a common source of resistance derived from ILC‐72. Disease reactions of the parents and RILs were scored using a 1 to 9 scale and also by using the area under the disease progress curve (AUDPC). Segregation among RILs indicated that three recessive and complementary major genes with several modifiers conferred ascochyta blight resistance. Absence of one or two of the major genes confers susceptibility, whereas the presence of the modifiers determines the degree of resistance.

No abstract

Evolutionary relationships were inferred among a worldwide sample of Ascochyta fungi from wild and cultivated legume hosts based on phylogenetic analyses of DNA sequences from the ribosomal internal transcribed spacer regions (ITS), as well as portions of three protein-coding genes: glyceraldehyde-3-phosphate-dehydrogenase (G3PD), translation elongation factor 1-alpha (EF) and chitin synthase 1 (CHS). All legume-associated Ascochyta species had nearly identical ITS sequences and clustered with other Ascochyta, Phoma and Didymella species from legume and nonlegume hosts. Ascochyta pinodes (teleomorph: Mycosphaerella pinodes [Berk. & Blox.] Vestergen) clustered with Didymella species and not with well characterized Mycosphaerella species from other hosts and we propose that the name Didymella pinodes (Berk. & Blox.) Petrak (anamorph: Ascochyta pinodes L.K. Jones) be used to describe this fungus. Analysis of G3PD revealed two major clades among legume-associated Ascochyta fungi with members of both clades infecting pea ("Ascochyta complex"). Analysis of the combined CHS, EF and G3PD datasets revealed that isolates from cultivated pea (P. sativum), lentil (Lens culinaris), faba bean (Vicia faba) and chickpea (Cicer arietinum) from diverse geographic locations each had identical or similar sequences at all loci. Isolates from these hosts clustered in well supported clades specific for each host, suggesting a co-evolutionary history between pathogen and cultivated host. A. pisi, A. lentis, A. fabae and A. rabiei represent phylogenetic species infecting pea, lentil, faba bean and chickpea, respectively. Ascochyta spp. from wild relatives of pea and chickpea clustered with isolates from related cultivated hosts. Isolates sampled from big-flower vetch (Vicia grandiflora) were polyphyletic suggesting that either this host is colonized by phylogenetically distinct lineages of Ascochyta or that the hosts are polyphyletic and infected by distinct evolutionary lineages of the pathogen. Phylogenetic species identified among legume-associated Ascochyta spp. were fully concordant with previously described morphological and biological species.