Mapping quantitative resistance to septoria tritici blotch in spelt wheat

The foliar wheat disease septoria tritici blotch can cause significant yield losses. A source of resistance has been mapped on chromosome 7D of spelt wheat, Triticum aestivum L. subsp. spelta (L.) Thell. The microsatellite-based genetic map was constructed from a set of 87 single-chromosome recombinant doubled-haploid lines bred from the cross between the landrace ‘Chinese Spring’ and a ‘Chinese Spring’-based line carrying chromosome 7D from spelt wheat. Two regions of the chromosome were associated with isolate-specific QTL expressed one at the seedling and another at the adult plant stage. The seedling resistance locus QStb.ipk-7D1 was found in the centromeric region of chromosome 7D, which corresponds to the location of the major resistance genes Stb4 originating from bread wheat cultivar ‘Tadinia’ and Stb5 originating from Triticum tauschii. The adult resistance locus QStb.ipk-7D2 was found on the short arm of chromosome 7D in a similar position to the locus Lr34/Yr18 known to be effective against multiple pathogens. Composite interval mapping confirmed QStb.ipk-7D1 and QStb.ipk-7D2 to be two distinct loci.     

Quantitative Trait Loci Analysis and Mapping of Seedling Resistance to Stagonospora nodorum Leaf Blotch in Wheat

ABSTRACT Stagonospora nodorum leaf blotch is an economically important foliar disease in the major wheat-growing areas of the world. In related work, we identified a host-selective toxin (HST) produced by the S. nodorum isolate Sn2000 and determined the chromosomal location of the host gene (Snn1) conditioning sensitivity to the toxin using the International Triticeae Mapping Initiative mapping population and cytogenetic stocks. In this study, we used the same plant materials to identify quantitative trait loci (QTL) associated with resistance to fungal inoculations of Sn2000 and investigate the role of the toxin in causing disease. Disease reactions were scored at 5, 7, and 10 days postinoculation to evaluate changes in the degree of effectiveness of individual QTL. A major QTL was identified on the short arm of chromosome 1B, which coincided with the snn1 toxin-insensitivity gene. This locus explained 58% of the phenotypic variation for the 5-day reading but decreased to 27% for the 10-day reading, indicating that the toxin is most effective in the early stages of the interaction. In addition, relatively minor QTL were identified on chromosomes 3AS, 3DL, 4AL, 4BL, 5DL, 6AL, and 7BL, but not all minor QTL were significant for all readings and their effects varied. Multiple regression models explained from 68% of the phenotypic variation for the 5-day reading to 36% for the 10-day reading. The Chinese Spring nullisomic 1B tetrasomic 1D line and the Chinese Spring-Triticum dicoccoides disomic 1B chromosome substitution line, which were insensitive to SnTox1, were more resistant to the fungus than the rest of the nullisomictetrasomic and disomic chromosome substitution lines. Our results indicate that the toxin produced by isolate Sn2000 is a major virulence factor.     

Genetic control of resistance to fenpropimorph in Ustilago maydis

Fenpropimorph-resistant mutants of Ustilago maydis were obtained at high frequency (30 × 10⁻⁶) after UV-irradiation followed by selection on media containing fenpropimorph (50 μ g mL⁻¹). Genetic analysis of 30 such mutants resulted in the identification of two unlinked chromosomal loci, the U/fpm -1 locus with two allelic genes ( U/fpm- 1A and U/fpm -1B) and the U/fpm -2 locus. The mutant genes U/fpm- 1A and U/fpm -2 are responsible for high resistance levels (Rf: 75–100 or 257–286 based on MICs or ED_50s, respectively), while the U/fpm -1B mutation gives only a small reduction (approximately 7–10-fold) in fenpropimorph sensitivity. Cross-resistance studies with other SBIs showed that the major gene ( U/fpm- 1A and U/fpm -2) mutants were cross-resistant to the related compound fenpropidin (Rf: 15–20 or 53–66 based on MICs or ED_50s values, respectively) and to tridemorph (Rf: 5 or 7.1–9.5 based on MICs or ED_50s values, respectively), but not to the inhibitors of steps of ergosterol biosynthesis preceding the Δ¹⁴-reductase. The minor gene ( U/fpm -1B) mutants also had low-level resistance (approximately 5-fold) to tridemorph and to fenpropidin, but in contrast with the major gene mutants they were 2–10 times more sensitive to the triazoles studied (triadimefon, triadimenol, propiconazole and flusilazole) and to the pyridine, pyrifenox.
Studies of the fitness of U. maydis mutants showed that in major gene mutants, resistance was not associated with changes in growth rate in liquid culture or pathogenicity on young maize plants. The minor gene mutation reduced significantly the growth rate in liquid culture and the pathogenicity, either in homozygous or heterozygous condition in dikaryotic mycelium.     

Main effects, epistasis, and environmental interactions of quantitative trait Loci for fusarium head blight resistance in a recombinant inbred population

ABSTRACT Chinese Spring Sumai 3 chromosome 7A disomic substitution line (CS-SM3-7ADS) is highly resistant to Fusarium head blight (FHB), and an F(7) population of recombinant inbred lines derived from the cross CS-SM3-7ADS x Annong 8455 was evaluated for resistance to FHB to investigate main effects, epistasis, and environmental interactions of quantitative trait loci (QTLs) for FHB resistance. A molecular linkage map consists of 501 simple sequence repeat and amplified fragment length polymorphism markers. A total of 10 QTLs were identified with significant main effects on the FHB resistance using MapQTL and QTLMapper software. Among them, CS-SM3-7ADS carries FHB-resistance alleles at five QTLs on chromosomes 2D, 3B, 4D, and 6A. One QTL on 3BS had the largest effect and explained 30.2% of the phenotypic variance. Susceptible QTLs were detected on chromosomes 1A, 1D, 4A, and 4B. A QTL for enhanced FHB resistance was not detected on chromosome 7A of CS-SM3-7ADS; therefore, the increased FHB resistance in CS-SM3-7ADS was not due to any major FHB-resistance QTL on 7A of Sumai 3, but more likely was due to removal of susceptible alleles of QTLs on 7A of Chinese Spring. QTLMapper detected nine pairs of additive-additive interactions at 17 loci that explained 26% phenotypic variance. QTL-environment interactions explained 49% of phenotypic variation, indicating that the environments significantly affected the expression of the QTLs, especially these epistasis QTLs. Adding FHB-enhancing QTLs or removal of susceptible QTLs both may significantly enhance the degree of wheat resistance to FHB in a wheat cultivar.     

Multiple fungicide resistance to benzimidazoles, dicarboximides and diethofencarb in field isolates of Botrytis cinerea in Israel

During the period January-March 1989, 15 greenhouses at 12 sites in Israel were surveyed for the presence of fungicide-resistant strains of Botrytis cinerea , using a fungicide-amended Botrytis -selective medium. Resistance to benzimidazoles (Ben^R) and to dicarboximides (Dic^R) was frequent in most sites. Resistance to carbendazim + diethofencarb (Ben^R NPC^R) was found in all eight sites in which a mixture of these fungicides had been used against grey mould, but not in other sites. A new phenotype of multiple fungicide resistance was found among these isolates. The new phenotype, designated Ben^R Dic^R NPC^R, combines the three previously described characteristics of resistance to benzimidazole, dicarboximide and N -phenylcarbamate fungicides. It was found only in cucumber greenhouses that had been sprayed with the fungicide mixture carbendazim + diethofencarb against grey mould. Isolates of this phenotype were pathogenic in artificial inoculation of cucumber cotyledons treated with carbendazim, iprodione or carbendazim + diethofencarb.     

Genome-wide association study for spot blotch resistance in Afghan wheat germplasm

Spot blotch (SB), caused by Bipolaris sorokiniana, is a devastating disease of wheat globally, especially in South Asia and South America. Understanding the genetics of resistance to SB is important for developing breeding strategies to improve resistance. A panel of 301 genotypes from Afghanistan was phenotyped over two crop seasons using a mixture of virulent B. sorokiniana isolates and genotyped using DArTSeq to obtain genome-wide markers. Fifty genotypes (16.6%) showed disease scores less than the resistant control. Principal component analysis using the genotypic data clustered the genotypes into five different groups. Among models used for genome-wide association mapping, the multilocus mixed model, and fixed and random model circulating probability unification algorithms were most effective in identifying significant marker-trait associations (MTA). Twenty-five MTAs at p ≤ .001 were identified on chromosomes 1A, 1B, 1D, 2B, 2D, 3A, 3B, 4A, 5A, 5B, 6A, 7A, and 7D, indicating the quantitative nature of resistance to SB. Phenotypic variation explained by these markers ranged from 2.0% to 17.7%, and genomic regions on the chromosomes 1D, 2D, 3A, 3B, 4A, 5A, and 5B coincided with loci identified in previous studies. Three single nucleotide polymorphism (SNP) markers on chromosomes 1B (SNP 1113207) and 5A (SNPs 5411867 and 998276) were significant in both crop seasons as well as in the combined analysis across seasons. Marker 5411867 is close to Vrn-A1, shown to be associated with SB in previous studies. Furthermore, among known SB resistance genes, Sb2 on chromosome 5B was predicted to be significant in this panel.     

Allelism of rice blast resistance genes in two Chinese rice cultivars, and identification of two new resistance genes

Blast, caused by Pyricularia grisea , is a major constraint on rice production. To broaden genetic diversity for resistance to this disease, two rice cultivars, GA20 and GA25 from Yunnan Province, China, were analysed for the genetic basis of their high resistance to blast. GA20 was crossed with 10 Japanese differential cultivars, and GA25 was crossed with nine of them and with the susceptible Chinese cultivar Lijiangxintuanheigu (LTH). The resistance of GA20 was governed by two dominant genes allelic to genes at the Pi-k and Pi-ta loci. The allele at the Pi-k locus was new, based on a reaction pattern different from known alleles at this locus. It could not be shown whether or not the allele at the Pi-ta locus is new, because races with virulence for Pi-ta were not tested. GA25 has one resistance gene, which is not allelic to genes at the loci Pi-a , Pi-k , Pi-z , Pi-ta , Pi-b , and Pi-t , but is linked to the Pi-i gene on chromosome 9 with a recombination frequency of 15.1 ± 2.8%.
The new allele at the Pi-k locus in GA20 is designated as Pi-k^g (t), and the new resistance gene in GA25 as Pi15(t) .     

Biocontrol of seedborne Botrytis cinerea in chickpea with Gliocladium roseum

An isolate of Gliocladium roseum proved highly antagonistic to Botrytis cinerea . Sporulation of B. cinerea on chickpea seed naturally infected or inoculated with B. cinerea was suppressed by seed treatment with conidial suspensions of G. roseum at 10⁷ and 10⁸ conidia/mL, respectively. Establishment of healthy seedlings in punnets (small trays) 5 weeks after sowing with inoculated seed was increased from 29.2% to 59.7% by treatment with G. roseum at 3×10⁷ conidia/mL, and from 1.4% to 69.4% with G. roseum at 3×10⁸ conidia/mL, the latter being equivalent to disease control by Thiram. There was no significant effect of Rhizobium on disease suppression by G. roseum , and treatment with G. roseum at 10⁸ conidia/mL did not reduce nodulation. Amendment with culture filtrates of G. roseum did not affect the growth rate of B. cinerea on potato dextrose agar, indicating that constitutive production of an antibiotic is not involved in biocontrol. A selective medium was developed to enumerate propagules of G. roseum on seed recovered from soil. There was no significant change in the population of G. roseum on seed after incubation for 4 weeks in soil to which the isolate of G. roseum was indigenous.     

Resistance to diethofencarb (NPC) in benomyl-resistant field isolates of Botrytis cinerea

Based on the 'negative cross-resistance' phenomenon between N -phenylcarbamates and benzimidazole fungicides, the fungicidal mixture of carbendazim + diethofencarb (MBC + NPC) was introduced, to control Botrytis cinerea phenotypes which are either sensitive to benzimidazoles and resistant to NPC (wild-type: Ben^S NPC^R). or resistant to benzimidazoles and sensitive to NPC(Ben^R NPC^S). At one out of four sites where the MBC + NPC mixture was used in commercial cucumber greenhouses, grey mould control failed and a new phenotype of B. cinerea was found. The new phenotype was resistant to benzimidazoles, as was 100% of the population screened in the four sites, but retained resistance to NPC. Accordingly, the new phenotype was designated Ben^R NPC^R. It was pathogenic on cucumber seedlings.     

Negative cross resistance between benzimidazole and N-phenylcarbamate fungicides and control of Botrytis cinerea on grapes

Isolates of Botrytis cinerea resistant to benzimidazoles (Ben^R), dicarboximides (Dic^R), or both (Ben^R Dic^R) were found on table grapes in vineyards in Israel. In vineyards treated for one or two seasons with benomyl and dicarboximides, 41% of the isolates were benomyl-resistant, 18% were dicarboximide-resistant and 21 % were resistant to both fungicides. The frequency of resistant strains was very low in non-treated vineyards. Negatively correlated cross resistance (NCCR) was manifested by 46 Ben^R isolates which were sensitive to isopropyl N -(3,4-diethoxyphenyl) carbamate (NPC) and 73 benomyl-sensitive (Ben^s) isolates which were insensitive to NPC; NCCR was not influenced by sensitivity to dicarboximides. A mixture of Ben^s Dic^R plus Ben^R Dic^s isolates, inoculated on rose petals, was inhibited by mixtures of benzimidazoles plus NPC but not by benomyl, NPC or iprodione alone. Grey mould, incited on maturing grape berries by a vineyard population composed of Ben^s and Ben^R strains, was not controlled by benomyl, while the mixture of NPC plus carbendazim was effective.     

Synthesis of the solanapyrone phytotoxins by Ascochyta rabiei in response to metal cations and development of a defined medium for toxin production

The phytotoxic solanapyrones A, B and C, were produced by Ascochyta rabiei when grown on Czapek Dox nutrients supplemented with an aqueous extract of chickpea seed but not when grown on Czapek Dox nutrients alone. Addition of amino acids, vitamins and inorganic ions to Czapek Dox nutrients allowed the production of the solanapyrones in good yields. By systematic elimination of components of this medium, the constituents essential for toxin production were identified as the divalent metal cations Zn²⁺, Ca²⁺, Mn²⁺ and Cu²⁺. When these ions were added to Czapek Dox nutrients in the same concentrations as those found in chickpea extract, concentrations of the phytotoxins similar to those found in Czapek Dox nutrients supplemented with chickpea extract were detected. Removal of cations from the chickpea supplement by a cation exchange resin did not affect the growth of the fungus compared with growth on the medium containing the complete supplement, but no toxin was produced. A defined medium and cultural conditions suitable for solanapyrone production by A. rabiei are described.     

Genetic Analysis of Deltamethrin Resistance in Laboratory-Selected Strains of Drosophila melanogaster MEIG

The genetic basis of deltamethrin resistance or sensitivity in two strains of Drosophila melanogaster was studied by means of chromosomal analysis. Eight homozygote combinations of resistant (SR) and sensitive (HS₁) strains were constructed by chromosome substitution and were tested using topical bioassay and electrophysiological tests. The analysis of the data showed that resistance to lethal effects was multigenic, with the major factor(s) located on the first (X) and second chromosomes. One significant positive interaction between the two chromosomes was also found. For the resistance to knockdown (measured by time-based topical test), the second chromosome was found to be much more important than the first and third chromosomes. However, analysis of the onset of the deltamethrin-induced electrical activity for each constructed strain suggested that reduced nerve sensitivity (probably associated to the deltamethrin resistance) was linked to both chromosomes X and 2. Similarly, bursts of large excitatory junctional currents (which were observed in sensitive and wild strains following topical application of deltamethrin) were not observed in resistant strains when these two chromosomes originated from the SR strain. A good correlation was found between the latency and LD₅₀ suggesting that the same factors might be involved in the electrophysiological effects and the lethal effects. In our strains, resistance most probably corresponds to reduced nerve sensitivity. Our data are consistent with the location of the sodium channel gene in Drosophila on the chromosome X but clearly demonstrate that this major gene cannot by itself explain target site resistance to deltamethrin.     

Evaluation of bacterial wilt resistance in tomato lines nearly isogenic for the Mi gene for resistance to root-knot

Resistance to bacterial wilt, caused by Ralstonia solanacearum , in tomato lines CRA 66 and Caraïbo is reported to be decreased by root-knot nematode galling and by introduction of the Mi gene for nematode resistance. The Mi gene is located on tomato chromosome 6, which also carries a major quantitative trait locus (QTL) for resistance to bacterial wilt. Bacterial wilt resistance was evaluated in F3-progenies derived from two crosses between near-isogenic lines, Caraïbo × Carmido and CRA 66 × Cranita, differing for small and large introgressions from Lycopersicon peruvianum that carry the Mi gene, respectively. These introgressed regions were mapped using RFLP markers. Plants homozygous Mi⁺/Mi⁺ (susceptible to the nematode) and homozygous Mi/Mi (resistant) for the Mi gene were selected in F2 and used to produce F3 progenies. Parents and F3-lines with Mi/Mi had resistance to bacterial wilt reduced by 30% in Caraïbo × Carmido and by 15% in CRA 66 × Cranita. Caraïbo and Carmido were demonstrated to be isolines and the small introgression from L. peruvianum resulted in loss of the QTL for bacterial wilt resistance, which is probably allelic or linked in repulsion to the Mi gene. In contrast, resistance to bacterial wilt segregated in the F3 lines from the cross CRA 66 × Cranita, giving families varying in resistance between the levels shown by the parents. Consequently, two hypotheses were considered: (i) after only four backcrosses, the parents were not isolines and the genes for resistance to bacterial wilt from CRA 66 were still segregating, and (ii) the parents were isolines and variation in resistance to bacterial wilt in F3 was due to recombination events among the large L. peruvianum introgressed chromosome region from Cranita.     

Chromosomal location and genetic relationship of leaf rust resistance genes rph9 and rph12 in barley

ABSTRACT Barley lines Hor 2596 and Triumph are the sources of leaf rust resistance genes Rph9 and Rph12, respectively. An allelism test was performed with F(2) progeny of the cross Triumph/Hor 2596 inoculated with Puccinia hordei. No recombinants were found in a population of 3,858 progeny, indicating Rph9 and Rph12 are alleles. Molecular and morphological markers were used to identify the chromosomal location of these genes in the crosses Bowman/Hor 2596 and Triumph/I91-533-va. A linkage was detected between Rph9 and the flanking sequence-tagged site (STS) markers ABC155 and ABG3 on chromosome 7(5H) at a distance of 20.6 and 20.1 centimorgans (cM), respectively, and to the microsatellite marker dehydrin-9 (HVDHN9) at a distance of 10.2 cM in the Bowman/ Hor 2596 cross. Analysis of isozymes in bulks of the same population showed that Rph9 may be closely linked to the Est9 locus on chromosome 7(5H). The Rph12 locus was linked to the morphological trait locus va (controlling variegated leaf color) on chromosome 7(5H) at a distance of 22.6 cM in the Triumph/I91-533-va cross. Rph12 also was linked with STS marker ABC155 (24.4 cM) and RAPD marker OPA19 (1.5) (17.8 cM). These data indicate that Hor 2596 and Triumph carry a leaf rust resistance gene at the same locus on the long arm of chromosome 7(5H) of barley.     

Influence of the d2 factor on survival and infection by the Dutch elm disease pathogen Ophiostoma ulmi

A particular form of mycovirus, the d² factor, which attacks the elm pathogen Ophiostoma ulmi, was found to be extremely deleterious to this fungus both in vitro and in vivo. Most significantly, d²-infected conidia were poor at persisting in feeding grooves, the usual infection court of the pathogen, and also showed a 50-fold reduction in successful xylem infection compared with their healthy counterparts. In addition, transmission of the d² factor from diseased to healthy isolates of O. ulmi was found to take place in feeding grooves, indicating that the fungus exists in a mycelial phase prior to invading xylem vessels.     

Identification and Mapping of Quantitative Trait Loci Conditioning Resistance to Southern Leaf Blight of Maize Caused by Cochliobolus heterostrophus Race O

ABSTRACT A random set of recombinant inbred (RI) lines (F2:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 simple sequence repeat, restriction fragment length polymorphism, or isozyme loci. Field plots of the RI lines were inoculated artificially with an aggressive isolate of C. heterostrophus race O in each of two growing seasons in North Carolina. Lines were rated for percent SLB severity two (1996) or three (1995) times during the grain-filling period. Data also were converted to area under the disease progress curve (AUDPC) and analyzed using the composite interval mapping option of the PLABQTL program. When means of disease ratings over years were fitted to models, a total of 11 quantitative trait loci (QTLs) were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTLs accounted for 46% of the phenotypic variation for resistance. QTL x environment interactions often were highly significant but, with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome 1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected, and accounted for most of the phenotypic variance. No significant additive x additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to SLB of maize.     

Sensitivity of Phytophthora infestans to flumorph: in vitro determination of baseline sensitivity and the risk of resistance

The sensitivity of 127 Phytophthora infestans isolates to flumorph was determined in 2003 and 2004. The isolates originated from two geographical regions and showed similar levels of sensitivity in both years. Baseline sensitivities were distributed as a unimodal curve with EC₅₀ values for growth of mycelia ranging from 0·1016 to 0·3228  µ g mL⁻¹, with a mean of 0·1813 (± 0·0405) µ g mL⁻¹. There was no cross-resistance between flumorph and metalaxyl. Laboratory studies were conducted to evaluate the risk of P. infestans developing resistance to flumorph. Mutants resistant to metalaxyl or flumorph were obtained by treating mycelium of wild-type isolates with ultraviolet radiation. Metalaxyl-resistant mutants were obtained with a high frequency and exhibited resistance factor values (EC₅₀ resistant/EC₅₀ sensitive phenotypes) of more than 100, while flumorph-resistant mutants were obtained at much lower frequencies and had very small resistance factors (1·5–3·2). There was cross-resistance between flumorph and dimethomorph, but not with azoxystrobin or cymoxanil. Most flumorph-resistant mutants showed decreases in hyphal growth in vitro and in sporulation both in vitro and on detached leaf tissues. These studies suggested that the risk of resistance developing was much lower for flumorph than metalaxyl. However, as P. infestans is a high-risk pathogen, appropriate precautions against resistance development should be taken.     

Resynthesis of multiple resistance to organophosphorus insecticides from strains with factors of resistance isolated from the SKA strain of house flies

Individual factors of resistance to insecticides attributable to chromosomes II, III and ^V of the SKA strain of houseflies (Musca domestica L) were combined in pairs to determine how their presence affects resistance. The re-synthesised strains with resistance factors on chromosomes II and V, and on chromosomes III and V, were tested with several organophosphorus insecticides and DDT. The penetration delaying mechanism Pen on chromosome III, which alone gives little or no resistance, slightly increased the resistance of flies with the microsomal detoxifying factor Ses on chromosome V to diazinon and malaoxon-ethyl (c. × 1.5), but was more effective in increasing resistance to DDT (× 6). There was no effect on the response to other insecticides tested. The combined effect of the mechanisms of resistance on chromosome II (glutathione S-ethyl transferase and phosphatase) and on chromosome V (microsomal detoxication) approximated to the product of the resistance conferred by each of these mechanisms singly, suggesting that the mechanisms of resistance on the two chromosomes act independently. Therefore, most of the strong resistance to organophosphorus insecticides in the SKA strain results from the interaction between delayed penetration (chromosome III) and the factors of resistance on chromosome II, and the independent action of the resistance factors on chromosomes II and V.     

Hydroxyproline-rich glycoprotein accumulation in tobacco leaves protected against Erysiphe cichoracearum by potato virus Y infection

Tobacco cv. Havana 425 acquired resistance to a compatible isolate of Erysiphe cichoracearum after infection by a strain of potato virus Y (PVY^N) that causes veinal necrosis; another common strain (PVY^O) that does not cause necrosis gave less protection. Hydroxyproline-rich glycoproteins (HRGPs), believed to be involved in resistance, were determined by analysing hydroxyproline (Hyp) in purified cell walls. Hyp content increased significantly in PVY^N-protected leaves, compared with untreated controls, 2–4 days after necrotic lesion symptoms developed. No further increase in Hyp was noted in PVY^N-protected leaves after E. cichoracearum challenge. Hyp increases were significantly higher in protected leaves of plants showing symptoms on day 7 than on day 10. Infection with the PVY^O strain caused significant decrease in Hyp content, compared with uninoculated controls. Inoculation of virus-free plants with E. cichoracearum induced moderate and transitory Hyp increases on day 2 or 3, followed by a quick decrease associated with a weak response by the compatible host. It is suggested that HRGP accumulation induced by PVY^N (but not by PVY^O) causes changes in the host cell wall that result in resistance to E. cichoracearum .     

小麦山农4143抗黑胚病遗传分析及抗性遗传位点检测

 黑胚病是小麦生产的重要籽粒病害,麦根腐平脐蠕孢(Bipolaris sorokiniana)是黑胚病的主要致病菌。为分析小麦抗黑胚病遗传规律并检测抗性位点,本研究以抗黑胚病小麦品系山农4143与感病品系宛原白1号的F₇代重组自交系(RIL)群体为材料,于2018~2019年在3个试验点种植,采用“孢子液喷洒、套袋保湿”的方法进行接菌鉴定,用“主基因＋多基因混合遗传模型”进行遗传分析,并挑选极端抗、感自交系构建混池、结合小麦660K SNP芯片进行混合分组分析(BSA)。研究结果显示小麦品系山农4143对黑胚病抗性符合“4对主基因加性-上位性遗传模型”,主基因遗传力为0.88~0.95;通过BSA检测到黑胚病抗性位点36个,分别位于1A、2B(6)、2D(2)、3A、3B(2)、3D、4A(6)、4D、5A(4)、5B(6)、5D(3)、7A、7B和7D共14条染色体上,A、B、D染色组上分别为13、 15和8个,36个位点中有18个为抗黑胚病新鉴定位点。本研究结果为小麦抗黑胚病位点的精细定位和抗性育种中分子标记的开发奠定了基础。