Preliminary investigation of QTLs associated with seedling resistance to ascochyta blight from <Emphasis Type="Italic">Cicer echinospermum</Emphasis>, a wild relative of chickpea

Accessions from Cicer echinospermum, a wild relative of chickpea (Cicer arietinum L.), contain resistance to the fungal disease ascochyta blight, a devastating disease of chickpea. A linkage map was constructed based on an interspecific F(2) population, derived from a cross between a susceptible chickpea cultivar (Lasseter) and a resistant C. echinospermum accession (PI 527930). The linkage map incorporated 83 molecular markers, that included RAPD, ISSR, STMS and RGA markers; eight markers remained unlinked. The map comprised eight linkage groups and covered a map distance of 570 cM. Six out of the eight linkage groups were correlated to linkage groups from the integrated Cicer map using STMS markers. Quantitative trait loci (QTLs) associated with ascochyta blight resistance were detected using interval mapping and single-point analysis. The F(2) population was evaluated for seedling and stem resistance in glasshouse trials. At least two QTLs were identified for seedling resistance, both of which were located within linkage group 4. Five markers were associated with stem resistance, four of which were also associated with seedling resistance. QTLs from previous studies also mapped to LG 4, suggesting that this linkage group is an important region of the Cicer genome for resistance to ascochyta blight.     

QTL analysis for ascochyta blight resistance in an intraspecific population of chickpea (<Emphasis Type="Italic">Cicer arietinum</Emphasis> L.)

In both controlled environment and the field, six QTLs for ascochyta blight resistance were identified in three regions of the genome of an intraspecific population of chickpea using the IDS and AUDPC disease scoring systems. One QTL-region was detected from both environments, whereas the other two regions were detected from each environment. All the QTL-regions were significantly associated with ascochyta blight resistance using either of the disease scoring systems. The QTLs were verified by multiple interval mapping, and a two-QTL genetic model with considerable epistasis was established for both environments. The major QTLs generally showed additive gene action, as well as dominance inter-locus interaction in the multiple genetic model. All the QTLs were mapped near a RGA marker. The major QTLs were located on LG III, which was mapped with five different types of RGA markers. A CLRR-RGA marker and a STMS marker flanked QTL 6 for controlled environment resistance at 0.06 and 0.04 cM, respectively. Other STMS markers flanked QTL 1 for field resistance at a 5.6 cM interval. After validation, these flanking markers may be used in marker-assisted selection to breed for elite chickpea cultivars with durable resistance to ascochyta blight. The tight linkage of RGA markers to the major QTL on LG III will allow map-based cloning of the underlying resistance genes.Communicated by P. Langridge     

Genetic mapping of ascochyta blight resistance in chickpea (Cicer arietinum L.) using a simple sequence repeat linkage map.

Ascochyta blight, caused by the fungus Ascochyta rabiei (Pass.) Lab., is one of the most devastating diseases of chickpea (Cicer arietinum L.) worldwide. Research was conducted to map genetic factors for resistance to ascochyta blight using a linkage map constructed with 144 simple sequence repeat markers and 1 morphological marker (fc, flower colour). Stem cutting was used to vegetatively propagate 186 F2 plants derived from a cross between Cicer arietinum L. 'ICCV96029' and 'CDC Frontier'. A total of 556 cutting-derived plants were evaluated for their reaction to ascochyta blight under controlled conditions. Disease reaction of the F1 and F2 plants demonstrated that the resistance was dominantly inherited. A Fain's test based on the means and variances of the ascochyta blight reaction of the F3 families showed that a few genes were segregating in the population. Composite interval mapping identified 3 genomic regions that were associated with the reaction to ascochyta blight. One quantitative trait locus (QTL) on each of LG3, LG4, and LG6 accounted for 13%, 29%, and 12%, respectively, of the total estimated phenotypic variation for the reaction to ascochyta blight. Together, these loci controlled 56% of the total estimated phenotypic variation. The QTL on LG4 and LG6 were in common with the previously reported QTL for ascochyta blight resistance, whereas the QTL on LG3 was unique to the current population.     

A linkage map of chickpea (Cicer arietinum L.) based on populations from Kabuli × Desi crosses: location of genes for resistance to fusarium wilt race 0

Two recombinant inbred line (RIL) populations derived from intraspecific crosses with a common parental line (JG62) were employed to develop a chickpea genetic map. Molecular markers, flower colour, double podding, seed coat thickness and resistance to fusarium wilt race 0 (FOC-0) were included in the study. Joint segregation analysis involved a total of 160 markers and 159 RILs. Ten linkage groups (LGs) were obtained that included morphological markers and 134 molecular markers (3 ISSRs, 13 STMSs and 118 RAPDs). Flower colour (B/b) and seed coat thickness (Tt/tt) appeared to be linked to STMS (GAA47). The single-/double-podding locus was located on LG9 jointly with two RAPD markers and STMS TA80. LG3 included a gene for resistance to FOC-0 (Foc0₁/foc0₁) flanked by RAPD marker OPJ20₆₀₀ and STMS marker TR59. The association of this LG with FOC-0 resistance was confirmed by QTL analysis in the CA2139 × JG62 RIL population where two genes were involved in the resistance reaction. The STMS markers enabled comparison of LGs with preceding maps.     

Characterization and genetic analysis of an EIN4-like sequence (CaETR-1) located in QTL(AR1) implicated in ascochyta blight resistance in chickpea

Two alleles of a chickpea (Cicer arietinum L.) ethylene receptor-like sequence (CaETR-1) were sequence-characterized using synteny analysis with genome sequences of Medicago truncatula L. The full length of the sequence obtained in the accession FLIP84-92C resistant to ascochyta blight (CaETR-1a) span 4,428?bp, including the polyadenylation signal in the 3'-untranslated region (UTR), whereas it has a 730?bp deletion in the 3'-UTR region in the susceptible accession PI359075 (CaETR-1b). The deduced protein belongs to subfamily II of the ethylene receptors and contains all the domains that define EIN4 homologs in Arabidopsis. The EIN4-like sequence (CaETR-1) has been mapped using a recombinant inbred line (RIL) population derived from an intraspecific cross between ILC3279 and WR315, resistant and susceptible to blight, respectively. The locus was located in LGIVa of the genetic map, flanked by markers NCPGR91 and GAA47 (at distances of 11.3 and 17.9?cM, respectively). This is the first potentially functional sequence identified under a QTL peak for ascochyta blight resistance in chickpea (QTL(AR1)). This EIN4-like (CaETR-1) sequence explained up to 33.8% of the total phenotypic variation. This sequence could be directly related to blight resistance, together with other QTLs that have been found to be involved in resistance to this major chickpea disease.     

Pathotype-specific genetic factors in chickpea (Cicer arietinum L.) for quantitative resistance to ascochyta blight

Ascochyta blight in chickpea (Cicer arietinum L.) is a devastating fungal disease caused by the necrotrophic pathogen, Ascochyta rabiei (Pass.) Lab. To elucidate the genetic mechanism of pathotype-dependent blight resistance in chickpea, F₇-derived recombinant inbred lines (RILs) from the intraspecific cross of PI 359075(1) (blight susceptible) × FLIP84-92C(2) (blight resistant) were inoculated with pathotypes I and II of A. rabiei. The pattern of blight resistance in the RIL population varied depending on the pathotype of A. rabiei. Using the same RIL population, an intraspecific genetic linkage map comprising 53 sequence-tagged microsatellite site markers was constructed. A quantitative trait locus (QTL) for resistance to pathotype II of A. rabiei and two QTLs for resistance to pathotype I were identified on linkage group (LG)4A and LG2+6, respectively. A putative single gene designated as Ar19 (or Ar21d) could explain the majority of quantitative resistance to pathotype I. Ar19 (or Ar21d) appeared to be required for resistance to both pathotypes of A. rabiei, and the additional QTL on LG4A conferred resistance to pathotype II of A. rabiei. Further molecular genetic approach is needed to identify individual qualitative blight resistance genes and their interaction for pathotype-dependent blight resistance in chickpea.     

QTL sequencing strategy to map genomic regions associated with resistance to ascochyta blight in chickpea

Whole‐genome sequencing‐based bulked segregant analysis (BSA) for mapping quantitative trait loci (QTL) provides an efficient alternative approach to conventional QTL analysis as it significantly reduces the scale and cost of analysis with comparable power to QTL detection using full mapping population. We tested the application of next‐generation sequencing (NGS)‐based BSA approach for mapping QTLs for ascochyta blight resistance in chickpea using two recombinant inbred line populations CPR‐01 and CPR‐02. Eleven QTLs in CPR‐01 and six QTLs in CPR‐02 populations were mapped on chromosomes Ca1, Ca2, Ca4, Ca6 and Ca7. The QTLs identified in CPR‐01 using conventional biparental mapping approach were used to compare the efficiency of NGS‐based BSA in detecting QTLs for ascochyta blight resistance. The QTLs on chromosomes Ca1, Ca4, Ca6 and Ca7 overlapped with the QTLs previously detected in CPR‐01 using conventional QTL mapping method. The QTLs on chromosome Ca4 were detected in both populations and overlapped with the previously reported QTLs indicating conserved region for ascochyta blight resistance across different chickpea genotypes. Six candidate genes in the QTL regions identified using NGS‐based BSA on chromosomes Ca2 and Ca4 were validated for their association with ascochyta blight resistance in the CPR‐02 population. This study demonstrated the efficiency of NGS‐based BSA as a rapid and cost‐effective method to identify QTLs associated with ascochyta blight in chickpea.     

Genetic marker discovery,intraspecific linkage map construction and quantitative trait locus analysis of ascochyta blight resistance in chickpea (Cicer arietinum L.)

Ascochyta blight, caused by the fungus Ascochyta rabiei (Pass.) Labr., is a highly destructive disease of chickpea (Cicer arietinum L.) on a global basis, and exhibits considerable natural variation for pathogenicity. Different sources of ascochyta blight resistance are available within the cultivated species, suitable for pyramiding to improve field performance. Robust and closely linked genetic markers are desirable to facilitate this approach. A total of 4,654 simple sequence repeat (SSR) and 1,430 single nucleotide polymorphism (SNP) markers were identified from a chickpea expressed sequence tag (EST) database. Subsets of 143 EST–SSRs and 768 SNPs were further used for validation and subsequent high-density genetic mapping of two intraspecific mapping populations (Lasseter × ICC3996 and S95362 × Howzat). Comparison of the linkage maps to the genome of Medicago truncatula revealed a high degree of conserved macrosynteny. Based on field evaluation of ascochyta blight incidence performed over 2 years, two genomic regions containing resistance determinants were identified in the Lasseter × ICC3996 family. In the S95362 × Howzat population, only one quantitative trait locus (QTL) region was identified for both phenotypic evaluation trials, which on the basis of bridging markers was deduced to coincide with one of the Lasseter × ICC3996 QTLs. Of the two QTL-containing regions identified in this study, one (ab_QTL1) was predicted to be in common with QTLs identified in prior studies, while the other (ab_QTL2) may be novel. Markers in close linkage to ascochyta blight resistance genes that have been identified in this study can be further validated and effectively implemented in chickpea breeding programs.     

Construction of a linkage map based on a <Emphasis Type="Italic">Lathyrus sativus</Emphasis> backcross population and preliminary investigation of QTLs associated with resistance to ascochyta blight

A linkage map of the Lathyrus sativus genome was constructed using 92 backcross individuals derived from a cross between an accession resistant (ATC 80878) to ascochyta blight caused by Mycosphaerella pinodes and a susceptible accession (ATC 80407). A total of 64 markers were mapped on the backcross population, including 47 RAPD, seven sequence-tagged microsatellite site and 13 STS/CAPS markers. The map comprised nine linkage groups, covered a map distance of 803.1 cM, and the average spacing between markers was 15.8 cM. Quantitative trait loci (QTL) associated with ascochyta blight resistance were detected using single-point analysis and simple and composite interval mapping. The backcross population was evaluated for stem resistance in temperature-controlled growth room trials. One significant QTL, QTL1, was located on linkage group 1 and explained 12% of the phenotypic variation in the backcross population. A second suggestive QTL, QTL2, was detected on linkage group 2 and accounted for 9% of the trait variation. The L. sativus R-QTL regions detected may be targeted for future intergenus transfer of the trait into accessions of the closely related species Pisum sativum.     

Improving chickpea yield by incorporating resistance to ascochyta blight

Ascochyta blight [Ascochyta rabiei (Pass.) Lab.] is the most destructive disease of chickpea (Cicer arietinum L.), but it can be managed effectively by the use of resistant cultivars. Therefore, a breeding programme was initiated during 1977–78 at ICARDA, Syria, to breed blight-resistant, high-yielding chickpeas with other desirable agronomic traits. Crosses were made in main season at Tel Hadya, Syria, and the F₁s were grown in the off season at Terbol, Lebanon. The F₂, F₄ and F₅ generations were grown in a blight nursery in the main season where blight epidemic was artificially created. The plants and progenies were scored for blight resistance and other traits. The F₃ and F₆ generations were grown in the off season under normal day length to eliminate late-maturing plants. The pedigree method of breeding was followed initially, but was later replaced by the F₄-derived family method. The yield assessment began with F₇ lines, first at ICARDA sites and later internationally. A total of 1584 ascochyta blight-resistant chickpea lines were developed with a range of maturity, plant height, and seed size not previously available to growers in the blight-endemic areas in the Mediterranean region. These included 92 lines resistant to six races of the ascochyta pathogen, and 15 large-seeded and 28 early maturity lines. New cultivars produced 33% more seed yield than the original resistant sources. The yield of chickpea declined by 340 kg ha^-1, with an increase in blight severity by one class on a 1–9 scale, reaching zero yield with the 8 and 9 classes. Development of blight-resistant lines made the introduction of winter sowing possible in the Mediterranean region with the prospect of doubling chickpea production. Twenty three cultivars have been released so far in 11 countries.Joint contribution from ICARDA and ICRISAT. ICRISAT Journal Article no. JA 1886.     

Genetic analyses and conservation of QTL for ascochyta blight resistance in chickpea (<Emphasis Type="Italic">Cicer arietinum</Emphasis> L.)

Ascochyta blight (AB) caused by Ascochyta rabiei (teleomorph, Didymella rabiei) Pass. Lab. is an important fungal disease of chickpea worldwide. Only moderate sources of resistance are available within the cultivated species and we hypothesized that the available sources may carry different genes for resistance, which could be pyramided to improve field resistance to AB. Four divergent moderately resistant cultivars CDC Frontier, CDC Luna, CDC Corinne, and Amit were each crossed to a highly susceptible germplasm ICCV 96029. Parents, F₁ and F₂ generations were evaluated under controlled conditions for their reactions to AB. A total of 144 simple sequence repeat (SSR) markers were first mapped to eight linkage groups (LG) for the CDC Frontier × ICCV 96029 population. Then based on the evidence from this population, 76, 61, and 42 SSR markers were systematically chosen and mapped in CDC Luna, CDC Corinne, and Amit populations, respectively. Frequency distributions of the AB rating in the F₂ generation varied among the four populations. Composite interval mapping revealed five QTLs (QTL1–5), one on each of LG 2, 3, 4, 6, and 8, respectively, distributed across different sources, controlling resistance to AB. CDC Frontier contained QTL2, 3, and 4 that simultaneously accounted for 56% of phenotypic variations. CDC Luna contained QTL 1 and 3. CDC Corinne contained QTL 3 and 5, while only QTL 2 was identified in Amit. Altogether these QTL explained 48, 38, and 14% of the estimated phenotypic variations in CDC Luna, CDC Corinne, and Amit populations, respectively. The results suggested that these QTLs could be combined into a single genotype to enhance field resistance to AB. Y. Anbessa and B. Taran contributed equally to this work.     

Genotyping with RAPD and microsatellite markers resolves pathotype diversity in the ascochyta blight pathogen of chickpea

 The poor definition of variation in the ascochyta blight fungus (Ascochyta rabiei) has historically hindered breeding for resistance to the chickpea (Cicer arietinum L.) blight disease in West Asia and North Africa. We have employed 14 RAPD markers and an oligonucleotide probe complementary to the microsatellite sequence (GATA)₄ to construct a genotype-specific DNA fragment profile from periodically sampled Syrian field isolates of this fungus. By using conventional pathogenicity tests and genome analysis with RAPD and microsatellite markers, we demonstrated that the DNA markers distinguish variability within and among the major pathotypes of A. rabiei and resolved each pathotypes into several genotypes. The genetic diversity estimate based on DNA marker analysis within pathotypes was highest for the least-aggressive pathotype (pathotype I), followed by the aggressive (pathotype II) and the most-aggressive pathotype (pathotype III). The pair-wise genetic distance estimated for all the isolates varied from 0.00 to 0.39, indicating a range from a clonal to a diverse relationship. On the basis of genome analysis, and information on the spatial and temporal distribution of the pathogen, a general picture of A. rabiei evolution in Syria is proposed. Received: 10 January 1998 / Accepted: 23 January 1998     

Molecular mapping of<Emphasis Type="Italic"> Fusarium oxysporum</Emphasis> f. sp.<Emphasis Type="Italic"> ciceris</Emphasis> race 3 resistance gene in chickpea

Sequence-tagged microsatellite site (STMS) and sequence-tagged site (STS) markers linked closely to Fusarium oxysporum f. sp. ciceris race 3 resistance gene in chickpea were identified, and linkage between three wilt resistance genes was elucidated. The resistance to race 3 in chickpea germplasm accession WR-315 was inherited as a single gene, designated foc-3, in 100 F₇ recombinant inbred lines derived from the cross of WR-315 (resistant) × C-104 (susceptible). The foc-3 gene was mapped 0.6 cM from STMS markers TA96 and TA27 and STS marker CS27A. Another STMS marker, TA194, at 14.3 cM, flanked the gene on the other side. Linkage between foc-3 and two other chickpea wilt resistance genes, foc-1 (syn. h ₁ ) and foc-4, was established. foc-3 was mapped 9.8 cM from foc-1 and 8.7 cM from foc-4, whereas foc-1 and foc-4 are closely linked at 1.1 cM. The identification of closely linked markers to resistance genes will facilitate marker-assisted selection for introgression of the race 3 resistance gene to susceptible chickpea lines.Communicated by H.C. Becker     

Quantitative trait locus mapping reveals conservation of major and minor loci for powdery mildew resistance in four sources of resistance in mungbean [Vigna radiata (L.) Wilczek]

Powdery mildew (PM) is a common and serious disease of mungbean [Vigna radiata (L.) Wilczek]. A few quantitative trait loci (QTL) for PM resistance in mungbean have been reported. The objective of this study was to locate QTL for PM resistance in two resistant accessions V4718 and RUM5. Simple sequence repeat markers were analyzed in an F₂ population from a cross between Kamphaeng Saen 1 (KPS1; susceptible to PM) and V4718 (resistant to PM), and in F₂ and BC₁F₁ populations from a cross between Chai Nat 60 (CN60; susceptible to PM) and RUM5 (resistant to PM). Progenies of 134 F_2:3 and F_2:4 lines derived from KPS1 × V4718, and 190 F_2:3 and 74 BC₁F_1:2 lines derived from CN60 × RUM5 and CN60 × (CN60 × RUM5), respectively, were evaluated for response to PM under field conditions. Multiple interval mapping identified a major QTL on linkage group (LG) 9 and two minor QTL on LG4 for the resistance in V4718, and detected two major QTL on LG6 and LG9 and one minor QTL on LG4 for the resistance in RUM5. Comparative linkage analysis of the QTL for PM resistance in this study and in previous reports suggests that the resistance QTL on LG9 in V4718, RUM5, ATF3640 and VC6468-11-1A are the same locus or linked. One QTL on LG4 is the same in three sources (V4718, RUM5 and VC1210A). Another QTL on LG6 is the same in two sources (RUM5 and VC6468-11-1A). In addition, one QTL in V4718 on LG4 appears to be a new resistance locus. These different resistance loci will be useful for breeding durably PM-resistant mungbean cultivars.     

Identification of quantitative trait loci and candidate genes for specific cellular resistance responses against Didymella pinodes in pea

Key message

Phenotyping of specific cellular resistance responses and improvement of previous genetic map allowed the identification of novel genomic regions controlling cellular mechanisms involved in pea resistance to ascochyta blight and provided candidate genes suitable for MAS.

Abstract

Didymella pinodes, causing ascochyta blight, is a major pathogen of the pea crop and is responsible for serious damage and yield losses. Resistance is inherited polygenically and several quantitative trait loci (QTLs) have been already identified. However, the position of these QTLs should be further refined to identify molecular markers more closely linked to the resistance genes. In previous works, resistance was scored visually estimating the final disease symptoms; in this study, we have conducted a more precise phenotyping of resistance evaluating specific cellular resistance responses at the histological level to perform a more accurate QTL analysis. In addition, P665 × Messire genetic map used to identify the QTLs was improved by adding 117 SNP markers located in genes. This combined approach has allowed the identification, for the first time, of genomic regions controlling cellular mechanisms directly involved in pea resistance to ascochyta blight. Furthermore, the inclusion of the gene-based SNP markers has allowed the identification of candidate genes co-located with QTLs and has provided robust markers for marker-assisted selection.     

Integration of sequence tagged microsatellite sites to the chickpea genetic map

Fifty sequence-tagged microsatellite site (STMS) markers and a resistant gene-analog (RGA) locus were integrated into a chickpea ( Cicer arietinum L., 2n = 2 x = 16 chromosomes) genetic map that was previously constructed using 142 F(6)-derived recombinant inbred lines (RILs) from a cross of C. arietinum x Cicer reticulatum Lad. The map covers 1,174.5 cM with an average distance of 7.0 cM between markers in nine linkage groups (LGs). Nine markers including the RGA showed distorted segregation ( P < 0.05). The majority of the newly integrated markers were mapped to marker-dense regions of the LGs. Six co-dominant STMS markers were integrated into two previously reported major quantitative trait loci (QTLs) conferring resistance to Ascochyta blight caused by Ascochyta rabiei (Pass.) Labr. Using common STMS markers as anchors, three maps developed from different mapping populations were joined, and genes for resistance to Ascochyta blight, Fusarium wilt (caused by Fusarium oxysporum Schlechtend.: Fr. f. sp. ciceris), and for agronomically important traits were located on the combined linkage map. The integration of co-dominant STMS markers improves the map of chickpea and makes it possible to consider additional fine mapping of the genome and also map-based cloning of important disease resistance genes.     

Restriction fragment length polymorphism analysis of loci associated with disease resistance genes and developmental traits in Pisum sativum L.

An F₂ population of pea (Pisum sativum L.) consisting of 174 plants was analysed by restriction fragment length polymorphism (RFLP) and random amplified polymorphic DNA (RAPD) techniques. Ascochyta pisi race C resistance, plant height, flowering earliness and number of nodes were measured in order to map the genes responsible for their variation. We have constructed a partial linkage map including 3 morphological character genes, 4 disease resistance genes, 56 RFLP loci, 4 microsatellite loci and 2 RAPD loci. Molecular markers linked to each resistance gene were found: Fusarium wilt (6 cM from Fw), powdery mildew (11 cM from er) and pea common Mosaic virus (15 cM from mo). QTLs (quantitative traits loci) for Ascochyta pisi race C resistance were mapped, with most of the variation explained by only three chromosomal regions. The QTL with the largest effect, on chromosome 4, was also mapped using a qualitative, Mendelian approach. Another QTL displayed a transgressive segregation, i.e. the parental line that was susceptible to Ascochyta blight had a resistance allele at this QTL. Analysis of correlations between developmental traits in terms of QTL effects and positions suggested a common genetic control of the number of nodes and earliness, and a loose relationship between these traits and height.     

A linkage map of the chickpea (Cicer arietinum L.) genome based on recombinant inbred lines from a C. arietinum×C. reticulatum cross: localization of resistance genes for fusarium wilt races 4 and 5

An integrated molecular marker map of the chickpea genome was established using 130 recombinant inbred lines from a wide cross between a cultivar resistant to fusarium wilt caused by Fusarium oxysporum Schlecht. emend. Snyd. &. Hans f. sp. ciceri (Padwick) Snyd & Hans, and an accession of Cicer reticulatum (PI 489777), the wild progenitor of chickpea. A total of 354 markers were mapped on the RILs including 118 STMSs, 96 DAFs, 70 AFLPs, 37 ISSRs, 17 RAPDs, eight isozymes, three cDNAs, two SCARs and three loci that confer resistance against different races of fusarium wilt. At a LOD-score of 4.0, 303 markers cover 2077.9 cM in eight large and eight small linkage groups at an average distance of 6.8 cM between markers. Fifty one markers (14.4%) were unlinked. A clustering of markers in central regions of linkage groups was observed. Markers of the same class, except for ISSR and RAPD markers, tended to generate subclusters. Also, genes for resistance to races 4 and 5 of fusarium wilt map to the same linkage group that includes an STMS and a SCAR marker previously shown to be linked to fusarium wilt race 1, indicating a clustering of several fusarium-wilt resistance genes around this locus. Significant deviation from the expected 1 : 1 segregation ratio was observed for 136 markers (38.4%, P<0.05). Segregation was biased towards the wild progenitor in 68% of the cases. Segregation distortion was similar for all marker types except for ISSRs that showed only 28.5% aberrant segregation. The map is the most extended genetic map of chickpea currently available. It may serve as a basis for marker-assisted selection and map-based cloning of fusarium wilt resistance genes and other agronomically important genes in future. Received: 17 November 1999 / Accepted: 4 June 2000     

Mapping quantitative trait loci in chickpea associated with time to flowering and resistance to Didymella rabiei the causal agent of Ascochyta blight

Drought is the major constraint to chickpea (Cicer arietinum L.) productivity worldwide. Utilizing early-flowering genotypes and advancing sowing from spring to autumn have been suggested as strategies for drought avoidance. However, Ascochyta blight (causal agent: Didymella rabiei (Kov.) v. Arx.) is a major limitation for chickpea winter cultivation. Most efforts to introgress resistance to the pathogen into Kabuli germplasm resulted in relatively late flowering germplasm. With the aim to explore the feasibility of combining earliness and resistance, RILs derived from a cross between a Kabuli cultivar and a Desi accession were evaluated under field conditions and genotyped with SSR markers. Three quantitative trait loci (QTLs) with significant effects on resistance were identified: two linked loci located on LG4 in epistatic interaction and a third locus on LG8. Two QTLs were detected for time to flowering: one in LG1 and another on LG2. When resistance and time to flowering were analyzed together, the significance of the resistance estimates obtained for the LG8 locus increased and the locus effect on days to flowering, previously undetected, was significantly different from zero. The identification of a locus linked both to resistance and time to flowering may account for the correlation observed between these traits in this and other breeding attempts.     

Identification of QTLs for resistance to powdery mildew and SSR markers diagnostic for powdery mildew resistance genes in melon (Cucumis melo L.)

Powdery mildew caused by Podosphaera xanthii is an important foliar disease in melon. To find molecular markers for marker-assisted selection, we constructed a genetic linkage map of melon based on a population of 93 recombinant inbred lines derived from crosses between highly resistant AR 5 and susceptible ‘Earl’s Favourite (Harukei 3)’. The map spans 877 cM and consists of 167 markers, comprising 157 simple sequence repeats (SSRs), 7 sequence characterized amplified region/cleavage amplified polymorphic sequence markers and 3 phenotypic markers segregating into 20 linkage groups. Among them, 37 SSRs and 6 other markers were common to previous maps. Quantitative trait locus (QTL) analysis identified two loci for resistance to powdery mildew. The effects of these QTLs varied depending on strain and plant stage. The percentage of phenotypic variance explained for resistance to the pxA strain was similar between QTLs (R ² = 22–28%). For resistance to pxB strain, the QTL on linkage group (LG) XII was responsible for much more of the variance (41–46%) than that on LG IIA (12–13%). The QTL on LG IIA was located between two SSR markers. Using an independent population, we demonstrated the effectiveness of these markers. This is the first report of universal and effective markers linked to a gene for powdery mildew resistance in melon.