Inheritance of resistance to Fusarium wilt (race 2) in chickpea

The inheritance of resistance to Fusarium wilt (race 2) of chickpea was studied in a set of three crosses, i.e. ‘WR315’בC104’ (resistant × susceptible), ‘WR315’בK850’ (resistant × tolerant) and ‘K850’בGW5/7’ (tolerant × tolerant) in order to investigate the number of genes involved, their complementation and to find out whether resistant segregants are possible in a cross between two tolerant cultivars. Tests of F₁, F₂ and F₃ generations of these crosses under controlled conditions at ICRISAT, Patancheru, India, indicated involvement of three loci (two recessive and one dominant alleles). The homozygous recessive form at the first two loci conferred resistance whereas susceptibility occurred when the first two loci were in the dominant form. A dominant allele at the third locus can complement the dominant alleles at the other two loci to confer tolerance. Occurrence of resistant segregants in a cross between two tolerant cultivars was observed.     

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.     

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.     

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.     

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.     

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 of resistance to Ascochyta blight in chickpea

Summary The mode of inheritance of resistance to Ascochyta blight (Ascochyta rabiei) isolate G-52 in chickpea was studied in three cross combinations and their reciprocals. It was found that resistance variety I-13 was controlled by a single dominant gene pair.     

Inheritance of resistance to Fusarium oxysporum f. sp. cubense race 1 in bananas

Fusarium wilt of bananas (also known as Panama disease), caused by the soil-borne fungus Fusarium oxysporum f. sp cubense (Foc), is a serious problem to banana production worldwide. Genetic resistance offers the most promising means to the control of Fusarium wilt of bananas. In this study, the inheritance of resistance in Musa to Foc race 1 was investigated in three F₂ populations derived from a cross between ‘Sukali Ndizi’ and ‘TMB2X8075-7’. A total of 163 F₂ progenies were evaluated for their response to Fusarium wilt in a screen house experiment. One hundred and fifteen progenies were susceptible and 48 were resistant. Mendelian segregation analysis for susceptible versus resistant progenies fits the segregation ratio of 3:1 (χ² = 1.72, P = 0.81), suggesting that resistance to Fusarium wilt in Musa is conditioned by a single recessive gene. We propose panama disease 1 to be the name of the recessive gene conditioning resistance to Fusarium wilt in the diploid banana ‘TMB2X8075-7’.     

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.     

Inheritance of resistance to Ascochyta rabiei in 15 chickpea germplasm accessions

Inheritance of resistance to race 4 of Ascochyta rabiei was studied in fifteen chickpea accessions known internationally for Ascochyta blight (AB) resistance. Resistance in ILC 200, ILC 5921, ILC 6043 and ILC 6090 was governed by a single recessive gene. Resistance in ILC 202 and ILC 2956 was conferred by two recessive complementary genes. In the case of ILC 5586, resistance was controlled by two dominant complementary genes and in the case of ILC 2506, two recessive genes with epistasis interaction were responsible for resistance. Resistance in ILC 3279, ILC 3856 and ILC 4421 was controlled either by three recessive genes or two recessives duplicated genes and in ILC 72, ILC 182 and ILC 187 resistance was polygenic in nature. The study provided insights into the genetics of Ascochyta blight resistance, and these could be used in crossing programmes to develop durable resistance. While the virulence spectrum of the pathogen in a region plays a crucial role in the deployment of resistance, ILC72, ILC182, ILC200, ILC442 and ILC6090 could provide acceptable level of resistance if incorporated into commercial cultivars.     

Resistance to Ascochyta blight in chickpea - Genetic basis

Summary Genetic regulation of host resistance in chickpea-Ascochyta rabiei interaction system is governed by two dominant complementary genes each in the genotypes GLG 84038 and GL 84099, whereas the resistance in a black seeded genotype ICC 1468 was controlled by one dominant and one recessive independent gene. In all the genotypes, resistance is operated by inter-allelic interactions. The genes conferring resistance in GLG 84038 were found to be different to those operating in GL 84099 and ICC 1468. Among the five dominant genes dispersed in 3 genotypes under study, at least one has been reported for the first time, as to date, only three dominant genes have been reported in the literature.The four identified dominant genes in GLG 84038 and GL 84099 have been named as Arc₁, Arc₂ (in GLG 84038) and Arc₃, Arc₄ (in GL 84099). The undistinguished dominant gene in ICC 1468 has been named as Arc_5(3,4) as it could not be equated or differentiated from Arc₃ or Arc₄. The recessive gene in ICC 1468 has been named as Arc₁.Generation mean analysis of the 6 resistant × susceptible crosses involving the same genotypes, revealed that the genes conferring resistance in any of the 3 genotypes did not follow simple Mendelian inheritance but were influenced by inter allelic interactions. Additive gene effect along with dominance were operative in all the 3 genotypes under study in conferring resistance. However, the mechanism of resistance in GLG 84038 and GL 84099 were primarily additive in nature while that in ICC 1468, dominance as well as dominance × dominance interactions were more important than additive gene action.     

中棉所12的黄萎病抗性遗传与育种应用研究

 以2个海岛棉品种和5个陆地棉品种为材料与中棉所12进行正反交,配制14个杂交组合的F₁和F₂ 。采用纸钵育苗,撕底伤根接种方法对14个组合的F₁和F₂群体进行黄萎病抗性鉴定。结果表明,以中棉所12作父本与海岛棉抗黄萎病品种或陆地棉抗黄萎病品种进行杂交,F₂抗（耐）病株与感病株的分离符合3：1的分离规律,说明海岛棉的抗黄萎病性对于中棉所12的耐黄萎病性为显性,中棉所12的耐黄萎病性对于陆地棉的感黄萎病性为显性,控制黄萎病抗性的基因为一个显性主基因。然而,以中棉所12为母本与海岛棉品种、抗病陆地棉品种和感病陆地棉品种进行杂交,F₂群体中90%以上的个体为抗病类型,说明中棉所12的细胞质中存在着抗黄萎病的遗传成分,具有细胞质母体遗传的特点,在棉花抗黄萎病育种中具有重要的利用价值。     

Inheritance of resistance to the 'Kanpur' race of Phytophthora drechsleri in pigeonpea

Phytophthora drechsleri causes stem blight, which is one of the most serious diseases of pigeonpea. Eight races of this fungus have been identified, but the inheritance of resistance to all these races is not clear except for race P2. This study examined the inheritance of resistance to race ‘Kanpur’ (KPR) of P. drechsleri in eight crosses involving four resistant parents, viz.‘KPBR 80‐2‐1′, ‘KPBR 80‐2‐2′, ‘Hy 3C and ‘BDN 1′, and two susceptible parents, viz.‘Bahar’ and ‘PDA 10′. The reactions of the parental lines, and their F₁, F₂ and backcross generations were studied in an infected plot. In the F₁ generation of all crosses, a susceptible reaction was observed that indicated dominance of susceptibility over resistance. The segregation pattern in F₂ indicated that two homozygous recessive genes (pdr₁pdr₁pdr₂pdr₂) were responsible for imparting resistance in the parents, ‘KPBR 80‐2‐1’ and ‘KPBR 80‐2‐2′, and that a single homozygous recessive gene (pdrpdr) was responsible for resistance in the parents ‘Hy 3C and ‘BDN 1′. Therefore, ‘KPBR 80‐2‐1’ and ‘KPBR 80‐2‐2’ with two genes for resistance are better donors because the resistance transferred from them will be more durable compared with ‘Hy3C and ‘BDN1’ with only one gene for resistance.     

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 Pseudomonas solanacearum E. F. Smith in Tetraploid Potato

Inheritance of bacterial wilt resistance in tetraploid potato was investigated in segregating progenies of parent clones with resistance derived from different specific sources and different types of adaptation. A race 1 and a race 3 isolate of Pseudomonas solanacearum were used to test the resistance under warm temperatures. Results obtained indicated partial dominance of resistance. Significant general and specific combining abilities showed that both additive and non-additive gene actions are important in conditioning resistance expression. There was evidence that epistasis is an important component of the non-additive gene action in the inheritance of resistance. Other aspects of the resistance and implications for breeding are discussed.     

丙基双氢茉莉酮酸酯诱导棉花耐黄萎病的效应

温室内以10mg·L 1的丙基双氢茉莉酮酸酯(PDJ)灌根预处理后,再用黄萎病菌(Verticilliumdahliae)孢子悬浮液接种棉苗,处理棉苗与对照相比发病率和病情指数有所降低,表现出对棉花黄萎病的耐病性。对一些生化指标进行测定发现,PDJ灌根和接种都可引起棉苗叶片中苯丙氨酸解氨酶(PAL)活性升高和木质素含量的增加,与此同时棉花叶片中的过氧化物酶(POD)活性及丙二醛(MDA)含量也都有所上升,在此基础上对PDJ诱导棉花耐黄萎病的可能生化机制作了归纳。     

Inheritance of a plant type mutant and its utilization in chickpea

Summary A macro-mutant, E 100Y(M) in chickpea (Cicer arietinum L.) was found to affect several plant and seed characters. For plant type monogenic inheritance was observed. A single pair of recessive genes pt/pt was ascribed to this mutant. The mutant locus seemed to be exerting pleiotropic action. The utilization of this mutant for chickpea improvement has been discussed.