Inheritance of resistance to fusarium wilt in chickpea

This preliminary study indicated that the resistance to race 2 of fusarium wilt is controlled by two genes, the first of which must be present in the homozygous recessive form, and the other in the dominant form, whether homozygous or heterozygous for complete resistance. Early wilting results if the other gene is homozygous recessive. Late wilting occurs if both loci are dominant. The existence of differences among chickpea cultivars in the time taken to express the initial symptoms of fusarium wilt were observed.     

Screening of Kabuli chickpea germplasm for resistance to Fusarium wilt

A total of 1915 Kabuli chickpea lines were screened in a wilt sick plot containing Fusarium oxysporum f.sp. ciceri race 0 at Béja, Tunisia. Complete resistance was found in 110 lines and this result was confirmed by a laboratory screening method. Principal components analysis showed that > 80% of the variation of the resistant lines was explained by hundred seed weight and days to maturity. Cluster analysis divided the resistant lines into four groups: 21 had high seed weight (48.25 ± 3.81 g) and early maturity (95.09 ± 2.50 d), 24 had high seed weight (46.84 ± 2.10 g) and late maturity (117.00 d), 34 had low seed weight (22.35 ± 4.72 g) and early maturity (92.97 ± 3.97 d) and 31 had low seed weight (19.62 ± 5.37 g) and late maturity (112.09 ± 4.51 d). This revised version was published online in July 2006 with corrections to the Cover Date.     

A second gene for resistance to race 4 of Fusarium wilt in chickpea and linkage with a RAPD marker

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.     

Inheritance and linkage of a gene for resistance to race 4 of fusarium wilt and RAPD markers in chickpea

Several races of Fusarium oxysporum Schlechtend.:Fr f. sp. ciceris (Padwick) Matuo and K. Sato cause economic losses from wilting disease of chickpea ( Cicer arietinum L.). While the genetics of resistance to race 1 have been reported, little is known of the genetics of resistance to race 4. We undertook a study to determine the inheritance of resistance and identified random amplified polymorphic DNA markers (RAPDs) linked to the gene for resistance. For the investigation, we used 100 F₅ derived F₇ recombinant inbred lines (RILs) that had been developed from the cross of breeding lines C-104 x WR-315. Results indicated that resistance is controlled by a single recessive gene. The RAPD markers previously shown to amplify fragments linked to race 1 resistance also amplified fragments associated with race 4 resistance. The RAPD loci, CS-27₇₀₀, UBC-170₅₅₀ and the gene for resistance to race 4 segregated in 1:1 ratios expected for single genes. Both RAPD markers were located 9 map units from the race 4 resistance locus and were on the same side of the resistance gene. Our results indicated that the genes for resistance to race 1 and 4 are 5 map units apart. The need to determine the genomic locations of race specific resistance genes and the possibility that these genes are clustered to the same genomic region should be investigated. This revised version was published online in July 2006 with corrections to the Cover Date.     

Two genes and linked RAPD markers involved in resistance to Fusarium oxysporum f. sp. Ciceris race 0 in chickpea

The inheritance of resistance to fusarium wilt race 0 of chickpea and linked random amplified polymorphic DNA (RAPD) markers were studied in two F₆:₇ recombinant inbred line (RIL) populations. These RILs were developed from the crosses CA2156 × JG62 (susceptible × resistant) and CA2139 × JG62 (resistant × resistant), and were sown in a field infected with fusarium wilt race 0 in Beja (Tunisia) over 2 years. A1:1 resistant to susceptible ratio was found in the RIL population from the CA2156 × JG62 cross, indicating that a single gene with two alleles controlled resistance. In the second RIL population (CA2139 × JG62) a 3:1 resistant to susceptible ratio indicated that two genes were present and that either gene was sufficient to confer resistance. Linkage analysis showed a RAPD marker, OPJ20600, linked to resistance in both RIL populations, which is present in the resistant parent JG62.     

Inheritance of resistance to flax wilt (Fusarium oxysporum f.sp. lini Schlecht) in a doubled haploid population of Linum usitatissimum L.

The inheritance of resistance to fusarium wilt (Fusarium oxysporum f.sp. lini) was investigated in Linum usitatissimum as a first step towards gaining an understanding of the molecular genetics of the disease and developing a procedure for marker-assisted selection. A recombinant doubled haploid (DH) population was derived from the haploid component of polyembryonic F₂ seeds originating from a cross between a wilt resistant, twinning Linola™ Linola is a registered trademark of CSIRO line CRZY8/RA91 and the wilt susceptible Australian flax cultivar Glenelg. The segregation of resistance was studied in 143 DH lines under glasshouse and field conditions. Most of the phenotypic variation was attributable to the segregation of two independent genes with additive effects. Minor resistance genes may have also contributed by modifying the resistance response. A glasshouse screening method of DH lines proved a reliable indicator of field resistance to fusarium wilt. This revised version was published online in July 2006 with corrections to the Cover Date.     

Fusarium vascular wilt in lentil: Inheritance and identification of DNA markers for resistance

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. F_2:4 progenies and F_6:8, F_6:9 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.     

Screening for resistance in wild Lycopersicon species to Fusarium oxysporum f.sp. lycopersici race 1 and race 2

Wild Lycopersicon accessions were screened for resistance to the Fusarium wilt disease caused by Fusarium oxysporum f.sp. lycopersici (Fol) race 1 and race 2. In total, four isolates of each race were used. Among 17 accessions of six Lycopersicon species tested, a wide genetic variation for wilt resistance was observed. Most accessions were highly susceptible, some showed intermediate resistance, but one accession of L. cheesmanii (G1.1615 = PI 266375) and two accessions of L. chilense (G1.1556 and G1.1558) were highly resistant to Fol races 1 and 2. The resistance in the latter three accessions equalled or was higher than the resistance determined by the known I-genes, that have been widely used in breeding programmes. These newly found resistant accessions provide breeders with more opportunities for Fusarium disease resistance and may contribute to our understanding of Fusarium disease resistance gene organisation and evolution.     

Genetic analysis of Fusarium wilt resistance in cowpea (Vigna unguiculata Walp.)

This study investigated the inheritance of resistance to Fusarium oxysporum f.sp. tracheiphilum (Fot) in cowpea lines. Resistant and susceptible cowpea lines were crossed to develop F₁, F₂ and backcross populations. Reaction to Fot was evaluated in 2015 and 2016 using seed soak and modified root‐dip inoculation methods. The expression of resistance reaction in the F₁ and segregation in F₂ generations indicated the role of dominant gene controlling Fot in cowpea. These results were further supported by the result of backcross (BC₁P₁F₁ and BC₁P₂F₁) progeny tests. The backcross of F₁ with the resistant parent produced progeny that were uniformly resistant, whereas backcross of F₁ with the susceptible parent produced progeny that segregated into 1:1 ratio. The F₂ segregation ratio in the reciprocal cross showed no evidence of maternal effect in the inheritance of the resistance. Allelism test suggests that the gene for resistance in TVu 134 was the same in TVu 410 and TVu 109‐1. We also identified an SSR marker, C13‐16, that cosegregated with the gene conferring resistance to Fot in cowpea.     

Inheritance of growth vigour and its association with other characters in chickpea

Growth vigour plays an important role in the establishment of a normal crop. The F₂ population of a cross between high‐ and low‐growth vigour varieties of chickpea segregated into 15 high : 1 low growth vigour. The results for recombinant inbred lines and BC1P₂ showed a good fit to the expected 3 : 1 ratio. The results indicated that growth vigour is controlled by two genes with duplicate dominant epistasis. No gene has so far been identified for growth vigour in chickpea. Correlation between growth vigour and other characters showed that high growth vigour had significant negative correlation with days to first flower, days to 50% flowering, days to first pod and days to maturity.     

Inheritance of Dry Root Rot (Rhizoctonia bataticola) Resistance in Chickpea (Cicer arietinum)

The inheritance of resistance to dry root rot of chickpea caused by Rhizoctonia bataticola was studied. Parental F₁ and F₂ populations of two resistant and two susceptible parents, along with 49 F₁ progenies of one of the resistant × susceptible crosses were rested for their reaction to dry root rot using the blotting-paper technique. All F, plants of the resistant × susceptible crosses were resistant; the F₂ generation fitted a 3 resistant: 1 susceptible ratio indicating monogenic inheritance, with resistance dominant over susceptibility. F³ family segregation data confirmed the results. No segregation occurred among the progeny of resistant × resistant and susceptible × susceptible crosses.     

Inheritance of race 1.2 Fusarium wilt resistance in four melon cultivars

The resistance to Fusarium oxysporum f.sp. melonis (Fom) race 1.2 has been studied in melons, such as the Portuguese accession ‘BG-5384’ and in the Japanese ‘Shiro Uri Okayama’, ‘Kogane Nashi Makuwa’, and ‘C-211’, since a good characterization of the resistance is necessary before its introgression into commercial varieties. These four melon accessions showed a high level of resistance to races 0, 1, and 2 of Fom, indicating that the partial resistance to the race 1.2 previously detected may not have been race specific. To determine the mode of inheritance of the resistance to Fom race 1.2, the F₁, F₂, BCP_R, and BCP_S generations from the crosses between the four resistant accessions above and ‘Piel de Sapo’, a Fom race 1.2 susceptible melon, were developed. They were subsequently inoculated with two Fom isolates, one from the pathotype 1.2Y and the other from the pathotype 1.2W. The area under the disease progress curve was determined for each inoculated plant, and the data were analyzed. We show that the resistance seen in these accessions is polygenically inherited with a complex genetic control because many epistatic interactions were detected. The three epistatic effects; additivity × additivity, dominance × dominance, and dominance × additivity are present and significant, with differing magnitudes from one cross to the next. The relatively low heritabilities, and these epistatic effects make difficult the improvement of the resistance, from these sources, through a standard selection procedure.     

灰黄霉素对尖孢镰刀菌抑制作用的研究

为进一步扩展灰黄霉素的农业应用范畴,选择采自甜瓜、黄瓜、西瓜、苦瓜、辣椒和西红柿的不同专化型的10株致病性尖孢镰刀菌作为试验对象,系统研究了灰黄霉素对尖孢镰刀菌的抑制作用。分别采用抑菌圈法和抑菌率法,测定灰黄霉素对不同寄主来源的尖孢镰刀菌的抑制作用,并显微观察灰黄霉素对尖孢镰刀菌菌丝生长的影响。结果表明灰黄霉素对不同寄主来源的尖孢镰刀菌具有良好的广谱抑制作用,但对不同菌株抑制效果差异显著,其抑制中浓度IC50为0.42~2.81 mM。尖孢镰刀菌经4 mM灰黄霉素处理后,菌丝变得稀疏、畸形、膨大、扭曲,从而影响其生长。因此,灰黄霉素可用于开发防治作物枯萎病的新型生物农药。     

Inheritance of resistance to Fusarium wilt in Indian lentil germplasm (Lens culinaris Medik.)

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.     

Screening lentil for resistance to fusarium wilt: methodology and sources of resistance

Host-plant resistance is the best means to control the key disease of lentil-vascular wilt, caused by Fusarium oxysporum Schlecht. emend. Snyder & Hansen f.sp. lentis Vasudeva and Srinivasan. Systematic screening for resistance to lentil wilt was initiated in the field in 1993, in a wilt-sick plot in North Syria, with a core collection of 577 germplasm accessions from 33 countries. A subset (88 accessions) of mostly resistant accessions was re-screened in 1994. The most resistant accessions came from Chile, Egypt, India, Iran and Romania. Variation among accessions in the temporal pattern of wilting was analyzed. The limited wilting in resistant accessions followed a linear model through time, whereas the pattern for susceptible accessions was better described with an exponential model. This temporal variation emphasizes the need for repeated scoring during screening for resistance to lentil vascular wilt to identify ‘late-wilters’. To overcome spatial variation in inoculum density, the efficacy of using wilt scores from a systematically-repeated susceptible control in covariate analysis was tested. Covariance analysis significantly improved overall screening by 3% in 1993, but the improvement was non-significant in 1994. The results emphasize the relative uniformity of disease pressure in the wilt-sick plot and suggest that covariance analysis of a systematically arranged control will be of greater benefit in land which is less uniformly infected. This revised version was published online in July 2006 with corrections to the Cover Date.     

Apium graveolens PI 181714 is a source of resistance to Fusarium oxysporum f. sp. apii race 4 in celery (A. graveolens var. dulce)

Celery has little genetic diversity and is highly susceptible to the new fungal pathogen Fusarium oxysporum f. sp. apii (Foa) race 4. After screening an Apium graveolens germplasm collection for resistance to Foa race 4, we crossed celery cv. 'Challenger', which is Foa race 2-resistant but Foa race 4-susceptible and A. graveolens PI 181714, which is Foa races 2- and 4-resistant but non-celery type. After selfing F₁s, we screened the F₁S₁ for race 4-resistance and celery-type and then selfed selected F₁S₁. Greenhouse and field trials indicate that three selected F₁S₂ families (76–8-4, 76–8-27 and 76–8-36) are suitable as germplasm for celery breeders for resistance to Foa race 4. A F1S3 76–8–36-124 is either fixed or nearly so for resistance to Foa races 4 and 2. Furthermore, quantitative PCR indicates that PI 181714 is resistant, rather than tolerant, to Foa races 4 and 2, and that this resistance has been introgressed into F1S3 76–8–36-124.     

Molecular mapping of QTLs for resistance to Fusarium wilt (race 1) and Ascochyta blight in chickpea (Cicer arietinum L.)

Fusarium wilt (FW) and Ascochyta blight (AB) are two important diseases of chickpea which cause 100 % yield losses under favorable conditions. With an objective to validate and/or to identify novel quantitative trait loci (QTLs) for resistance to race 1 of FW caused by Fusarium oxysporum f. sp. ciceris and AB caused by Ascochyta rabiei in chickpea, two new mapping populations (F_2:3) namely ‘C 214’ (FW susceptible) × ‘WR 315’ (FW resistant) and ‘C 214’ (AB susceptible) × ‘ILC 3279’ (AB resistant) were developed. After screening 371 SSR markers on parental lines and genotyping the mapping populations with polymorphic markers, two new genetic maps comprising 57 (C 214 × WR 315) and 58 (C 214 × ILC 3279) loci were developed. Analysis of genotyping data together with phenotyping data collected on mapping population for resistance to FW in field conditions identified two novel QTLs which explained 10.4–18.8 % of phenotypic variation. Similarly, analysis of phenotyping data for resistance to seedling resistance and adult plant resistance for AB under controlled and field conditions together with genotyping data identified a total of 6 QTLs explaining up to 31.9 % of phenotypic variation. One major QTL, explaining 31.9 % phenotypic variation for AB resistance was identified in both field and controlled conditions and was also reported from different resistant lines in many earlier studies. This major QTL for AB resistance and two novel QTLs identified for FW resistance are the most promising QTLs for molecular breeding separately or pyramiding for resistance to FW and AB for chickpea improvement.