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1.
Fusarium wilt caused by Fusarium oxysporum Schlechtend.: Fr f. sp. ciceris (Padwick) Matuo & Sato is a devastating disease of chickpea. The current study was conducted to determine the inheritance of the gene(s) for resistance to race 4 of fusarium wilt and to identify linked RAPD markers using an early wilting line, JG-62, as a susceptible parent. Genetic analysis was performed on the F1s, F2s and F3 families from the cross of JG-62 × Surutato-77. The F3 families were inoculated with a spore suspension of the race 4 wilt pathogen and the results were used to infer the genotypes of the parent F2 plants. Results indicated that two independent genes controlled resistance to race 4. Linkage analysis of candidate RAPD marker, CS-27700, and the inferred F2 phenotypic data showed that this marker locus is linked to one of the resistance genes. Allelism indicated that the two resistance sources, Surutato-77 and WR-315, shared common alleles for resistance and the two susceptible genotypes, C-104 and JG-62, carried alleles for susceptibility. The PCR-based marker, CS-27700, was previously reported to be linked to the gene for resistance to race 1 in a different population which suggested that the genes for resistance to races 1 and 4 are in close proximity in the Cicer genome. This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   

2.
Fusarium wilt is an economically important disease of tomatoes, caused by the soil-born fungus Fusarium oxysporum f. sp. lycopersici. There are three host-specific races of this pathogen. The dominant tomato gene I-2 confers resistance to race 2. The I-2 fusarium resistance gene was mapped genetically to chromosome 11 of tomato, between the RFLP markers TG105 and TG36, 0.4 centiMorgan (cM) from TG105. A mean value of 43 kb for each cM was assigned in the vicinity of I-2. We have generated new RFLP markers in the region by chromosome walking from TG105 towards I-2 on lambda clones, and by subcloning a 350 kb long YAC clone (YAC 8) that contains TG105. These RFLP markers were mapped physically on YAC 8 by PFGE. The location of I-2 relative to these markers was genetically estimated using a recombinant inbred (RI) segregating population. The order of the markers according to the RI population is inconsistent with their order on the physical map. A cDNA clone, D14, that was isolated by YAC 8, turned out to be 53% similar to xanthine dehydrogenase from mammals and flies. Antibodies raised against a part of the protein encoded by D14 recognize cross reacting material of MW 80 kD, that is highly enriched in nodules of legumes, and seems to be induced by various environmental and pathogenic stress conditions.  相似文献   

3.
Chickpea (Cicer arietinum L.) production has remained static for the past two decades. One major limiting factor has been susceptibility of cultivars to several biotic and abiotic stresses that adversely affect yield. In recent years, cultivars resistant to Ascochyta blight (Ascochyta rabiei [Pass.] Lab.), Fusarium wilt (Fusarium oxysporum f. sp. ciceris), and cold have been bred and released in many countries. Some progress has been made in breeding for resistance to drought, insects, and cyst nematode, but not for viruses, heat, and salinity. Two or more stresses are of equal importance in most chickpea growing areas. Therefore, future efforts should be directed toward the development of cultivars with multiple-stress resistance. Proper understanding of important stresses in different countries and the genetics of resistance should lead to more systematic approaches to resistance breeding. Wild Cicer species hold promise and deserve attention in resistance breeding.  相似文献   

4.
Ascochyta blight (AB) caused by Ascochyta rabiei, is globally the most important foliar disease that limits the productivity of chickpea (Cicer arietinum L.). An intraspecific linkage map of cultivated chickpea was constructed using an F2 population derived from a cross between an AB susceptible parent ICC 4991 (Pb 7) and an AB resistant parent ICCV 04516. The resultant map consisted of 82 simple sequence repeat (SSR) markers and 2 expressed sequence tag (EST) markers covering 10 linkage groups, spanning a distance of 724.4 cM with an average marker density of 1 marker per 8.6 cM. Three quantitative trait loci (QTLs) were identified that contributed to resistance to an Indian isolate of AB, based on the seedling and adult plant reaction. QTL1 was mapped to LG3 linked to marker TR58 and explained 18.6% of the phenotypic variance (R 2) for AB resistance at the adult plant stage. QTL2 and QTL3 were both mapped to LG4 close to four SSR markers and accounted for 7.7% and 9.3%, respectively, of the total phenotypic variance for AB resistance at seedling stage. The SSR markers which flanked the AB QTLs were validated in a half-sib population derived from the same resistant parent ICCV 04516. Markers TA146 and TR20, linked to QTL2 were shown to be significantly associated with AB resistance at the seedling stage in this half-sib population. The markers linked to these QTLs can be utilized in marker-assisted breeding for AB resistance in chickpea.  相似文献   

5.
Fusarium wilt, caused by Fusarium oxysporum f. sp. melonis (F.o.m), is a worldwide soil-borne disease of melon (Cucumis melo L.). The most effective control measure available is the use of resistant varieties. Resistance to races 0 and 2 of this fungal pathogen is conditioned by the dominant gene Fom-1. An F2 population derived from the ‘Charentais-Fom1’ × ‘TRG-1551’ cross was used in combination with bulked segregant analysis utilizing the random amplified polymorphic DNA (RAPD) markers, in order to develop molecular markers linked to the locus Fom-1. Four hundred decamer primers were screened to identify three RAPD markers (B17649, V01578, and V061092) linked to Fom-1 locus. Fragments amplified by primers B17649 and V01578 were linked in coupling phase to Fom1, at 3.5 and 4 cM respectively, whereas V061092 marker was linked in repulsion to the same dominant resistant allele at 15.1 cM from the Fom-1 locus. These RAPDs were cloned and sequenced in order to design primers that would amplify only the target fragment. The derived sequence characterized amplified region (SCAR) markers SB17645 and SV01574 (645 and 574 bp, respectively) were present only in the resistant parent. The SV061092 marker amplified a band of 1092 bp only in the susceptible parent. These markers are more universal than the CAPS markers developed by Brotman et al. (Theor Appl Genet 10:337–345, 2005). The analysis of 24 melon accessions, representing several melon types, with these markers revealed that different melon types behaved differently with the developed markers supporting the theory of multiple, independent origins of resistance to races 0 and 2 of F.o.m.  相似文献   

6.
When challenged with Fusarium oxysporum f. sp. vasinfectum (Fov) from vegetative compatibility groups (VCGs) 01111 and 01112 in glasshouse tests, Gossypium australe Mueller and Gossypium sturtianum Willis accessions showed a variety of disease responses ranging from highly resistant to highly susceptible. Under high disease pressure G. sturtianum accession Gos-5275 was significantly more resistant than the commercial G. hirsutum cultivars that are designated standards for Fusarium resistance by Australian cotton breeders. Under low disease pressure G. sturtianum accession Gos-5250 was more susceptible than a highly susceptible commercial cultivar. A series of glasshouse tests was performed at two locations (Indooroopilly, QLD. and Canberra, ACT), and under low and high disease pressure. In these tests, a hexaploid cross (Gos-5271) generated from a Fusarium-resistant G. sturtianum (Gos-5275) and a Fusarium-susceptible G. hirsutum L. (CPI-138969) was significantly more resistant to Fusarium wilt than its G. hirsutum parent. Thus G. sturtianum, with a diploid genome and a range of responses to Fov challenge, has the potential to provide the basis for the elucidation of the genetic basis of resistance to Fusarium wilt in cotton species. In addition, resistant accessions of G. sturtianum are identified as a potential source of Fusarium wilt resistance genes for cotton breeding. In the glasshouse tests used to assess the resistance of various Gossypium accessions to Fusarium wilt disease, the scoring of vascular browning was found to give a more reliable indication of disease severity than the scoring of foliar symptoms. This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   

7.
Summary The latent periods, wilting rates and percentages of diseased plants were analyzed for 11 carnation cultivars after root and after stem inoculation with race 2 of Fusarium oxysporum f.sp. dianth. There was no conclusive evidence for the presence of an independent extravascular resistance mechanism, except for Lena plants in which, additional to the vascular resistance components, independent root-bound factors causing retardation of the colonization and wilting process were found. A large variation was observed in the ablity of the cultivars to localize the pathogen in the vascular tissue shortly after infection of the xylem. This ability was positively correlated with the latent period, and negatively with the wilting rate and final disease index. In resistant cultivars, secondary compartmentalization of the fungus higher up in the stem was also observed. After stem inoculation, differences among the cultivars in localization ability and wilt-retarding actors could be identified at an early stage by comparing the precentages of non-colonized plants or the percentages of plants lacking vascular discolouration.  相似文献   

8.
The aim of the present work was to determinate if resistant gene analogs (RGAs) previously identified and characterized by our group are involved in the early response to Fusarium oxysporum f. sp. ciceris (Foc). The expression profile of RGAs was determined using quantitative real-time polymerase chain-reaction (qPCR) in WR315 (resistant) and ILC3279 (susceptible) genotypes in response to Foc race 5 inoculation. Our results demonstrate that RGA05 and RGA07 were induced after Foc race 5 treatment at 2 days after inoculation (DAI) in the resistant genotype. In contrast RGA10 was induced in both resistant and susceptible plants, although the basal level of this gene was higher in the resistant genotype. On the contrary, no significant changes were observed for any of these genes at 7 DAI. Our results suggest a role of some of the candidate genes in the early response against fusarium wilt, mainly as part of the inducible defensive system. Thus, these genes could be a good start point for further studies such as candidate gene mapping or understand the bases for resistance in chickpea.  相似文献   

9.
Resistance of chickpea against the disease caused by the ascomycete Ascochyta rabiei is encoded by two or three quantitative trait loci, QTL1, QTL2 and QTL3. A total of 94 recombinant inbred lines developed from a wide cross between a resistant chickpea line and a susceptible accession of Cicer reticulatum, a close relative of cultivated chickpea, was used to identify markers closely linked to QTL1 by DNA amplification fingerprinting in combination with bulked segregant analysis. Of 312 random 10mer oligonucleotides, 3 produced five polymorphic bands between the parents and bulks. Two of them were transferred to the population on which the recent genetic map of chickpea is based, and mapped to linkage group 4. These markers, OPS06-1 and OPS03-1, were linked at LOD-scores above 5 to markers UBC733B and UBC181A flanking the major ascochyta resistance locus. OPS06-1 mapped at the peak of the QTL between markers UBC733B (distance 4.1 cM) and UBC181A (distance 9.6 cM), while OPS03-1 mapped 25.1 cM away from marker UBC733B on the other flank of the resistance locus. STMS markers localised on this linkage group were transferred to the population segregating for ascochyta resistance. Three of these markers were closely linked to QTL1. Twelve of 14 STMS markers could be used in both populations. The order of STMS markers was essentially similar in both populations, with differences in map distances between them. The availability of flanking STMS markers for the major resistance locus QTL1 will help to elucidate the complex resistance against different Ascochyta pathotypes in future. This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   

10.
Mapping genes for double podding and other morphological traits in chickpea   总被引：4，自引：0，他引：4  
Seed traits are important considerations for improving yield and product quality of chickpea (Cicer arietinum L.). The purpose of this study was to construct an intraspecific genetic linkage map and determine map positions of genes that confer double podding and seed traits using a population of 76 F10 derived recombinant inbred lines (RILs) from the cross of ‘ICCV-2’ (large seeds and single pods) × ‘JG-62’ (small seeds and double podded). We used 55 sequence-tagged microsatellite sites (STMS), 20 random amplified polymorphic DNAs (RAPDs), 3inter-simple sequence repeats (ISSR) and 2 phenotypic markers to develop a genetic map that comprised 14 linkage groups covering297.5 cM. The gene for double podding (s) was mapped to linkage group 6 and linked to Tr44 and Tr35 at a distance of7.8 cM and 11.5 cM, respectively. The major gene for pigmentation, C, was mapped to linkage group 8 and was loosely linked to Tr33 at a distance of 13.5 cM. Four QTLs for 100 seed weight (located on LG4 and LG9), seed number plant-1 (LG4), days to 50% flower (LG3) were identified. This intraspecific map of cultivated chickpea is the first that includes genes for important morphological traits. Synteny relationships among STMS markers appeared to be conserved on six linkage groups when our map was compared to the interspecific map presented by Winter et al. (2000). This revised version was published online in August 2006 with corrections to the Cover Date.  相似文献   

11.
Summary Soil-borne fungal diseases are among the most important factors, limiting the yield of grain legumes in many countries worldwide. Root rot, caused by Aphanomyces euteiches, Rhizoctonia solani, Fusarium solani and wilt, caused by several formae speciales of Fusarium oxysporum are the most destructive soil-borne diseases of pea, chickpea, lentil, fababean and lupin. The most effective control of these diseases is achieved through the use of resistant varieties. In this paper, recent advances in conventional and innovative screening methods for disease resistance are presented. Many grain legume accessions, which are maintained in national and international germplasm collections, have been evaluated for disease resistance and numerous resistant varieties have been released following incorporation of identified resistance genes from these sources. Recent identification of molecular markers tightly linked to resistance genes has greatly enhanced breeding programs by making marker assisted selection (MAS) possible and allowing the development of varieties with multiple disease resistance. Progress in the understanding of the biology of soil-borne fungal pathogens of grain legumes is also reviewed with particular reference to the genetic structure of their populations, diagnosis and host–pathogen interaction.  相似文献   

12.
A series of half-diallel crosses involving early, medium and late maturity desi and kabuli type chickpea (Cicer arietinum L.) genotypes with stable resistance to Helicoverpa pod borer, along with the parents, were evaluated at two locations in India to understand the inheritance of pod borer resistance and grain yield. Inheritance of resistance to pod borer and grain yield was different in desi and kabuli types. In desi type chickpea, the additive component of genetic variance was important in early maturity and dominance component was predominant in medium maturity group, while in the late maturity group, additive as well as dominance components were equally important in the inheritance of pod borer resistance. Both dominant and recessive genes conferring pod borer resistance seemed equally frequent in the desi type parental lines of medium maturity group. However, dominant genes were in overall excess in the parents of early and late maturity groups. In the kabuli medium maturity group, parents appeared to be genetically similar, possibly due to dispersion of genes conferring pod borer resistance and susceptibility, while their F1s were significantly different for pod borer damage. The association of genes conferring pod borer resistance and susceptibility in the parents could be attributed to the similarity of parents as well as their F1s for pod borer damage in kabuli early and late maturity groups. Grain yield was predominantly under the control of dominant gene action irrespective of the maturity groups in desi chickpea. In all the maturity groups, dominant and recessive genes were in equal frequency among the desi parental lines. Dominant genes, which tend to increase or decrease grain yield are more or less present in equal frequency in parents of the early maturity group, while in medium and late maturity groups, they were comparatively in unequal frequency in desi type. Unlike in desi chickpea, differential patterns of genetic components were observed in kabuli chickpea. While the dominant genetic component was important in early and late maturity group, additive gene action was involved in the inheritance of grain yield in medium duration group in kabuli chickpea. The dominant and recessive genes controlling grain yield are asymmetrically distributed in early and medium maturity groups in kabuli chickpea. The implications of the inheritance pattern of pod borer resistance and grain yield are discussed in the context of strategies to enhance pod borer resistance and grain yield in desi and kabuli chickpea cultivars.  相似文献   

13.
J. W. Scott  J. P. Jones 《Euphytica》1989,40(1-2):49-53
Summary Resistance to fusarium wilt, incited by Fusarium oxysporum (Schlecht.) f. sp. lycopersici (Sacc.) Snyder & Hansen race 3 in tomato (Lycopersicon esculentum Mill.) was discovered in LA 716, a L. pennellii accession. A resistant BC1F3 breeding line, E427, was developed from LA 716. E427 was crossed with the susceptible cv. Suncoast and F1, BCP1, BCP2 (to Fla 7155, a susceptible parent) F2, F3, and BCP2S1 seeds were obtained. Segregation for resistance following root dip inoculation over three experiments indicated a single dominant gene controlled resistance. Five of the 12 BCP1S1's segregated more susceptible plants, whereas one of the 12 segregated more resistant plants than expected (P<0.05). Three of 23 F3 lines segregated more susceptible plants than expected while 1 of the 23 had more resistant plants than expected (P<0.05). Segregation in all other lines fit expected ratios. Five of the 23 F3's were homozygous resistant which was an acceptable fit to expectations (P=0.1–0.5). The gene symbol I 3 is proposed for resistance to race 3 of the wilt pathogen. Deviations from expected ratios in data reported here and for other breeding lines indicate an effect of modifier genes and/or incomplete penetrance. Plant age at inoculation and seed dormancy did not affect results.Florida Agricultural Experiment Station Journal Series No. 8101.  相似文献   

14.
Botrytis grey mould (BGM) caused by Botrytis cinerea Pers. ex. Fr. is the second most important foliar disease of chickpea (Cicer arietinum L.) after ascochyta blight. An intraspecific linkage map of chickpea consisting of 144 markers assigned on 11 linkage groups was constructed from recombinant inbred lines (RILs) of a cross that involved a moderately resistant kabuli cultivar ICCV 2 and a highly susceptible desi cultivar JG 62. The length of the map obtained was 442.8 cM with an average interval length of 3.3 cM. Three quantitative trait loci (QTL) which together accounted for 43.6% of the variation for BGM resistance were identified and mapped on two linkage groups. QTL1 explained about 12.8% of the phenotypic variation for BGM resistance and was mapped on LG 6A. It was found tightly linked to markers SA14 and TS71rts36r at a LOD score of 3.7. QTL2 and QTL3 accounted for 9.5 and 48% of the phenotypic variation for BGM resistance, respectively, and were mapped on LG 3. QTL 2 was identified at LOD 2.7 and flanked by markers TA25 and TA144, positioned at 1 cM away from marker TA25. QTL3 was a strong QTL detected at LOD 17.7 and was flanked by TA159 at 12 cM distance on one side and TA118 at 4 cM distance on the other side. This is the first report on mapping of QTL for BGM resistance in chickpea. After proper validation, these QTL will be useful in marker-assisted pyramiding of BGM resistance in chickpea.  相似文献   

15.
Summary Three lentil genotypes resistant to Fusarium oxysporum f.sp. lentis viz. Pant L 234, JL 446 and LP 286 were crossed with two susceptible ones. The hybrid plants were all resistant in the eight crosses evaluated. Segregation pattern for wilt reaction in F2, BC(P1), BC(P2) and F3 generations in field and glasshouse conditions indicated that resistance to Fusarium wilt is under the control of two dominant duplicate genes in Pant L 234 and two independent dominant genes with complementary effects in JL 446 and LP 286. A third dominant gene complementary to the dominant genes in JL 446 and LP 286 is present in two susceptible lines. Allelic tests suggest the presence of five independently segregating genes for resistance. Duplicate dominant genes in Pant L 234 are non-allelic to two dominant genes with complementary effects in LP 286 and JL 446 and the third gene complementary to the two genes in JL 446 and LP 286 in susceptible lines JL 641 and L 9–12. Gene symbols among parental genotypes have been designated.  相似文献   

16.
Halo-blight is an important worldwide bacterial disease of common bean (Phaseolus vulgaris L.) caused by Pseudomonas syringae pv. phaseolicola. Nine races of the pathogen and five race-specific resistance genes have been previously described. However, a quantitative response to this pathogen has also been described. The objective of this study was to identify halo-blight resistance loci linked to molecular markers that could be used in resistance breeding. Chromosomal regions related to race 5 halo-blight resistance were localized on a genetic map of RAPD and AFLP molecular markers and constructed by the analysis of a “Jules” × “Canela” F2 progeny. “Jules” shows quantitative resistance to halo-blight and “Canela” is a very appreciated but susceptible Spanish bean landrace. Two QTL for resistance to halo-blight were mapped in two linkage groups. There were four large groups, with 14–22 molecular markers each, five with 4–8 markers each, and three with 2 or 3 markers each.  相似文献   

17.
Ascochyta blight is a major fungal disease affecting chickpea production worldwide. The genetics of ascochyta blight resistance was studied in five 5 × 5 half-diallel cross sets involving seven genotypes of chickpea (ICC 3996, Almaz, Lasseter, Kaniva, 24B-Isoline, IG 9337 and Kimberley Large), three accessions of Cicer reticulatum (ILWC 118, ILWC 139 and ILWC 184) and one accession of C. echinospermum (ILWC 181) under field conditions. Both F1 and F2 generations were used in the diallel analysis. The disease was rated in the field using a 1–9 scale. Almaz, ICC 3996 and ILWC 118 were the most resistant (rated 3–4) and all other genotypes were susceptible (rated 6–9) to ascochyta blight. Estimates of genetic parameters, following Hayman’s method, showed significant additive and dominant gene actions. The analysis also revealed the involvement of both major and minor genes. Susceptibility was dominant over resistance to ascochyta blight. The recessive alleles were concentrated in the two resistant chickpea parents ICC 3996 and Almaz, and one C. reticulatum genotype ILWC 118. The wild Cicer accessions may have different major or minor resistant genes compared to the cultivated chickpea. High narrow-sense heritability (ranging from 82% to 86% for F1 generations, and 43% to 63% for F2 generations) indicates that additive gene effects were more important than non-additive gene effects in the inheritance of the trait and greater genetic gain can be achieved in the breeding of resistant chickpea cultivars by using carefully selected parental genotypes.  相似文献   

18.
Barley genotypes Hor 1428, Hor 2926, Hor 3209, BBA 2890, Abyssinian 14, Grannelose Zweizeilige, and Stauffers Obersulzer are resistant to all races of Puccinia striiformis f. sp. hordei so far detected in the U.S.A. Heils Franken, Cambrinus, Astrix, Emir, Hiproly, Varunda, Trumpf,Mazurka, Bigo, BBA 2890, and I 5 are resistant to some races and susceptible to others. Previous studies showed that Hor 1428, Hor 2926, Hor 3209, Abyssinian 14, Stauffers Obersulzer, I 5, Heils Franken, Emir, Astrix, Hiproly, Varunda, and Trumpf each have two genes, and BBA 2890, Grannelose Zweizeilige, Cambrinus, Mazurka, Bigo, and BBA 809 each have a single genefor resistance. To determine the genes in specific genotypes and their relationships, all possible crosses were made among the 18 genotypes. Seedlings of parents and F2 progeny were tested under controlledconditions for resistance to selected races that were avirulent on both parents. Based on segregation within the individual crosses to selected races, at least 26 of 30 genes detected in the 18 genotypes were different. Allelic and linkage relationships of some of the genes were determined. The genetic information should be useful for understanding the host-pathogen interactions and for control of stripe rust using resistance.  相似文献   

19.
R. S. Pan  T. A. More 《Euphytica》1996,88(2):125-128
Summary Melon germplasm was screened for cucumber green mottle mosaic virus (CGMMV), powdery mildew (Sphaerotheca fuliginea), downy mildew (Pseudoperonospora cubensis) and Fusarium wilt (Fusarium oxysporum f. sp. melonis) resistance under artificial conditions except downy mildew for which screening was done under natural epiphytotic conditions. High level resistance to all the four diseases was not recorded in any of the collections tested. Nevertheless, ertheless, resistance to three diseases was located in three germplasm. Wild Cucumis species C. figarei exhibited absolute resistance to CGMMV and Fusarium wilt and high level resistance to downy mildew. Phoot or snapmelon (Cucumis melo var. momordica) — a non-dessert from of Indian origin—was highly resistant to downy mildew and resistant to CGMMV and medium resistant to Fusarium wilt. Iroquois was resistant to powdery mildew and medium resistant to downy mildew and CGMMV.  相似文献   

20.
Summary Effects of resistance genes and heat tolerance genes on expression of resistance to bacterial wilt caused by Pseudomonas solanacearum were investigated in 30 F1 progenies from parents with different levels of bacterial wilt resistance and heat tolerance. A race 1 and a race 3 isolate of the bacterium were used for inoculation under screenhouse conditions at two locations. Results obtained indicated that with reduction in levels of parental resistance, resistance in the F1 progenies was also reduced. Under hot conditions, a reduced heat tolerance in the genetic background also resulted in lower levels of resistance expression. The effect of heat tolerance tended to diminish at lower temperatures leaving the effect of resistance genes more consistent. There existed a strong interaction between resistance genes and genes for heat tolerance. The nature of resistance to bacterial wilt in potato and implications for breeding for resistance are discussed.Effects of reciprocal crosses on expression of resistance to a race 1 isolate under hot screenhouse conditions, were studied in 5 sets of reciprocal F1 progenies involving different resistant and susceptible parents. The reciprocal differences observed were not significant suggesting absence of cytoplasmic effects on expression of resistance.  相似文献   

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