Inheritance of Resistance to Powdery Mildew Race 2 in Citrullus lanatus var. lanatus

in HortScience

Information on the mode of inheritance of powdery mildew resistance in watermelon is important for designing a breeding strategy for the development of new cultivars. Resistance in the watermelon accession PI 270545 was investigated by generation means analysis by crossing it with susceptible PI 267677. The analyses showed involvement of two genes, a recessive resistance gene, pmr-1, and a dominant gene for moderate resistance, Pmr-2. Resistance to powdery mildew in the leaf had a large dominance effect and a heritability of 71%. The additive-dominance model was inadequate in explaining variation in leaf resistance as revealed by the joint scaling test. However, nonallelic interactions could not be detected by the nonweighted six-parameter scaling test. For stem resistance, the additive-dominance model was adequate, and inheritance was controlled mainly by additive effects. A high narrow-sense heritability of 79% suggested that selection for stem resistance in early generations would be effective.

Abstract

Information on the mode of inheritance of powdery mildew resistance in watermelon is important for designing a breeding strategy for the development of new cultivars. Resistance in the watermelon accession PI 270545 was investigated by generation means analysis by crossing it with susceptible PI 267677. The analyses showed involvement of two genes, a recessive resistance gene, pmr-1, and a dominant gene for moderate resistance, Pmr-2. Resistance to powdery mildew in the leaf had a large dominance effect and a heritability of 71%. The additive-dominance model was inadequate in explaining variation in leaf resistance as revealed by the joint scaling test. However, nonallelic interactions could not be detected by the nonweighted six-parameter scaling test. For stem resistance, the additive-dominance model was adequate, and inheritance was controlled mainly by additive effects. A high narrow-sense heritability of 79% suggested that selection for stem resistance in early generations would be effective.

Powdery mildew in watermelon [Citrullus lanatus (Thumb.) Matsum. and Nakai] caused by the fungus Podosphaera xanthii race 2W has in recent years become a concern among growers as well as plant breeders in United States (Davis et al., 2001; McGrath, 2001), China (Feng, 1996; Zhang et al., 2011), and other parts of the world (McGrath, 2001; Tomason and Gibson, 2006). The disease causes significant yield loss as well as decreased fruit quality (McGrath and Thomas, 1996) through mycelial coverage of the leaves, leaf necrosis, and premature death of the plant (Davis et al., 2001). Powdery mildew of watermelon occurs throughout the southeastern United States, extending north to New York as well as into western states (Davis et al., 2005).

Development of genetic resistance is an important objective in watermelon breeding programs. Screening of the U.S. watermelon germplasm collection identified high resistance in several wild accessions of C. lanatus var. citroides (Davis et al., 2007; Tetteh et al., 2010), but none of the accessions in the primary gene pool. However, one accession of C. lanatus var. lanatus, PI 270545, originating from Sudan was found to have intermediate resistance (Tetteh et al., 2010). Resistance in this accession was characterized by few mycelium on leaf and stem, and affected plants survived to fruit production stage (Tetteh et al., 2010).

To help breed cultivars resistant to powdery mildew, it is important to understand the inheritance and gene action. Tetteh et al. (2013) evaluated the gene action of leaf and stem resistance in the watermelon accession, PI 189225, and established that mainly additive gene action controlled leaf resistance, whereas for stem resistance, additive, dominance, and epistasic gene actions were significant. There are several reports on inheritance of resistance to P. xanthii in melon (Cucumis melo L.). Most agree that there are several genes controlling resistance (Epinat et al., 1993; Kenigsbuch and Cohen, 1992; McCreight, 2003; McCreight et al., 1987; Pitrat et al., 1998). Perchepied et al. (2005) working with quantitative trait loci (QTL) revealed that powdery mildew resistance in melon was under the control of major gene effects and digenic epistasis. Inheritance of powdery mildew resistance in watermelon was investigated by generation means analysis by Tetteh et al. (2013). Studies have demonstrated a close correspondence between generation mean analysis and QTL mapping (Jung et al., 1994; Perchepied et al., 2005).

Estimation of genetic effects in different crosses should inform the breeding strategy for development of resistant cultivars. Although additive and dominance models can be determined with the scaling tests in generation means analysis, the identification of non-allelic interactions requires more powerful tests such as the joint scaling test (Mather, 1949) or QTL analysis (Perchepied et al., 2005). In most cases, the variation unaccounted for by a major gene is provided by digenic epistasis.

A major deficiency of generation means is in nondetection of additive effects resulting from dispersion of alleles with similar effects between parents and internal cancellation of dominance effects exhibited in opposite directions at different loci (Crow and Kimura, 1970). Saudhu and Nittal (1988) studied two Gossypium arboreum crosses and reported the absence of nonallelic interaction in the six-parameter model, whereas the joint scaling test predicted the presence of epistasis for yield of seed cotton per plant (Iqbal and Nadeem, 2003).

Given the lack of genetic information on powdery mildew resistance in the primary gene pool of watermelon, a generation means analysis was carried out to determine inheritance, gene action, and heritability of resistance in PI 270545. Information on these parameters would be useful for designing an efficient breeding strategy for watermelon powdery mildew resistance.

Materials and Methods

Plant material.

A single population of watermelon segregating for resistance to powdery mildew race 2W-U.S. was derived from a cross between the susceptible P1 (PI 269677) and resistant P2 (PI 270545). The parents were inbred for two generations before crossing to produce plants uniform for powdery mildew resistance. From this, crosses were made to create a total of six generations, F1, F2, BC1P1 (the first backcross to P1), and BC1P2 (the first backcross to P2) for a study of inheritance of resistance.

Experimental design.

Seeds of inbred powdery mildew-resistant PI 270545 and -susceptible PI 269677, together with their F1, reciprocal F1, F2 (generated by self-pollination of the F1), and backcross generations were produced in 2007 to 2008 in greenhouses at the Department of Horticultural Science, North Carolina State University, Raleigh, NC. Seeds were planted in two sets, each consisting of 10 plants of each parent, 10 plants of F1, 10 plants of F1 reciprocal, 100 plants of F2, and 30 plants of each BC1. Pooled over sets, a total of 20 plants for each parent, 17 plants of F1, 19 of F1 reciprocal, 190 plants of the F2, and 59 plants each of BC1P1 and BC1P2 were evaluated for powdery mildew leaf and stem resistance, accounting for missing plants.

Seeds were planted in 100-mm pots containing 4P Fafard soilless mix (Conrad Fafard Incorporated, Agawam, MA) and arranged on greenhouse benches. Conditions of growth in the greenhouse were 16-h photoperiod, light intensity of 200 μmol·m−2·s−1, and 20 to 26 °C day and 13 to 19 °C night air temperature.

Inoculum production and seedling inoculation.

Seedlings were inoculated three times at weekly intervals, starting at the first true leaf stage. A spore suspension of Podosphaera xanthii race 2W-U.S. (4 × 104 conidia/mL) was sprayed over the plants until runoff. The suspension was prepared from inoculum isolated from infected commercial watermelon fields in South Carolina over the surface. After each inoculation, seedlings were maintained under plastic shading at 100% humidity for 7 d and subsequently at normal greenhouse conditions of 37% to 70% relative humidity and temperature of 24 to 38 °C (night to day).

Disease assessment.

Individual plants were rated for disease severity on a 0 to 9 scale on leaves and stems at 21 and 30 d after first inoculation. For leaf resistance rating, 0 = no symptoms; 1 = faint yellow speck on leaves; 2 = chlorotic lesions on leaves; 3 = chlorotic lesions covering 20% of leaves; 4 = yellow chlorotic lesions on leaves turned to brown necrotic areas; 5 = two to three healthy colonies of mycelium on leaves; 6 = less than 20% mycelium coverage on leaves; 7 = 20% to 50% mycelium coverage on leaves; 8 = 50% to 70% mycelium coverage with large necrotic areas; 9 = all leaves fully covered with powdery mycelium or plant dead. For stem resistance rating, 0 = no symptoms; 1 = first appearance of necrotic spots on stem; 2 = two to three necrotic spots on the stem; 3 = necrotic spots covering less than 10% of stem; 4 = first sign of active mycelium sporulation on stem; 5 = two to three healthy colonies of mycelium on stem; 6 = less than 20% mycelium coverage on stem; 7 = 20% to 50% mycelium coverage on stem; 8 = 50% to 70% mycelium coverage with large necrotic areas; 9 = entire stem fully covered with powdery mycelium or plant dead. On the basis of resistance levels of parental genotypes, plants were classified into two groups. In Group 1, plants having leaf and stem resistance ratings of 0 to 2 were classified as resistant, whereas ratings of 3 to 9 were classified as susceptible. Classification in Group 2 was based on ratings of 0 to 2 as resistant, 3 to 5 as moderately resistant, and 6 to 9 as susceptible.

Statistical analysis.

Generation means and variances were calculated. Variances for the two parents and reciprocal F1 were examined for correlation (data not shown). Correlation of variance with mean indicated a need for transformation of the data. A log10 transformation was applied but this did not reduce the correlation. A nonsignificant test of homogeneity of F1 and F1r variance demonstrated no maternal effect; hence, the two generations were pooled. Chi square was used to test the goodness of fit of the observed ratio of segregation to expected ratio in the F2 and backcross progenies. Analysis of variance was performed with generations as fixed effects and blocks (sets) as random effects. Phenotypic correlation between leaf and stem resistance was calculated. Data for each generation were pooled over replicates within each block. Generation means analysis was conducted on plot means by the ABC scaling test and the joint scaling test based on additive-dominance model (Cavalli, 1952; Mather and Jinks, 1971) in which the generations were subjected to a weighted least squares regression based on the equation:

article image
and a nonweighted scaling test based on the six-parameter model (Mather and Jinks, 1971). In this equation, Y is the mean of a given generation, m is the midpoint, d is the pooled additive effect, h is the pooled dominance effect, i is the additive × additive effect, j is the additive × dominance effect, l is the dominance × dominance effect, and a1 to a5 are the coefficients of the genetic effects in the equation (Carson and Hooker, 1981; Mather and Jinks, 1971). The significance of the joint scaling test, as tested by χ2, provided evidence of non-allelic interactions.

Narrow-sense heritability was calculated as

article image
where VF2 = variance among F2 plants of the single-cross population; and VBC1P1 and VBC1P2 are variances among plants from the backcrosses of F1 × P1 and F1 × P2 (Warner, 1952). A se of heritability h2 was derived as the square root of
article image

Results and Discussion

Faint specks of mycelium were observed 14 d after inoculation. On Day 21, disease development was poor with few patches of mycelium on few plants of the susceptible genotypes. On Day 30, major differences in disease scores for resistant, intermediate resistant, and susceptible plants were evident. Hence, disease ratings on Day 30 were used for all analyses. All plants of PI 270545 demonstrated resistance to moderate resistance with none showing absence of disease. The reaction of PI 269677 to P. xanthii was highly susceptible.

Table 1 shows the reactions of watermelon accessions to powdery mildew. For leaf rating, all plants of the resistant genotype were consistently rated between 1 and 3. None of the plants showed absence of disease. Of 20 plants, 25% scored 1, 55% scored 2, and 20% had a rating of 3, corresponding to 16 resistant and four moderately resistant plants. For stem resistance, 40% scored 0, 35% scored 1, 20% scored 2, and 5% scored 3, corresponding to 19 resistant and one moderately resistant plant. Thus, PI 270545 was between resistant and moderately resistant. All F1 plants were susceptible (Table 1) and F1 mean was greater than the midparent indicating dominance of the allele for susceptibility. Robinson et al. (1975) had earlier reported that high susceptibility to P. xanthii in PI 269677 was controlled by the single recessive gene, pm. The new and more virulent P. xanthii races on watermelon recently appear to exhibit different mode of inheritance.

Table 1.

Reactions of watermelon plants inoculated with powdery mildew race 2W-U.S isolate.

Table 1.

For leaf rating in the F2 progenies, there were 29 highly resistant, 40 moderately resistant, and 121 susceptible plants. A χ2 goodness-of-fit test on all three-category expected segregation ratios gave probability values < 0.01. However, the combination of moderately resistant with susceptible individuals fitted a 3:13 segregation ratio (Table 1) that was supported by a corresponding backcross segregation ratio of 1:3. The apparent model for this ratio was two genes with one recessive for high resistance and the other dominant for moderate resistance. The cumulative effect of the two genes in the F2 produced some highly resistant and some moderately resistant plants. Similar inheritance was observed for stem rating, in which the F2 gave a good fit for 3:13 model ( of 0.39, P = 0.53) supported by a backcross to the resistant parent of 1:3 ( f of 4.75; P = 0.03). This provided further evidence that two independent genes, one recessive and one dominant, control powdery mildew resistance in PI 270545. Occurrence of epistasis suggests that the dominant allele at one locus could mask the expression of alleles at the second, whereas the recessive allele at the second locus could mask the expression of the alleles at the first. The resistance genes found in PI 270545 were designated pmr-1 for the recessive gene for high resistance and Pmr-2 for the dominant gene for moderate resistance.

Analysis of variance (Table 2) revealed significant differences (P < 0.01) for both leaf and stem resistance among the generations, indicating the presence of genetic variability for both leaf and stem resistance. Variation was similar for both leaf and stem resistance. This is in contrast to the observation made on watermelon families of the PI 189225 resistant accession in which leaf resistance among the generations was higher than stem resistance (Tetteh et al., 2013). Comparison of means of P1 and P2 showed significant differences for both leaf and stem rating (Table 3). Disease development in F1 and F2 generations were not significantly different. Both had significantly lower (P < 0.05) disease development than the susceptible parent and were less resistant (P < 0.05) than the resistant parent (Table 3). These values were higher than the backcross to the resistant parent but lower than the backcross to the susceptible parent. Mean performance of the BC1P2 individuals showed more resistance to powdery mildew than the BC1P1. There was a highly significant correlation (r = 0.99, P < 0.0001) between leaf and stem resistance.

Table 2.

Mean squares for powdery mildew race 2W-U.S. leaf and stem resistance of generation mean analysis for the cross PI 269677 × PI 270545.

Table 2.
Table 3.

Mean, range, and se for leaf and stem powdery mildew race 2W-U.S. resistance ratings parents, F1, F2, and backcross generations of resistant × susceptible watermelons.

Table 3.

Leaf resistance.

In the generation means analysis, although the ABC scaling test (Table 4) was not significant, indicating that a simple additive-dominance model was adequate, the joint scaling test indicated a model that goes beyond additive-dominance for leaf resistance [ 564; P < 0.001]. Therefore, the six-parameter model was required to explain the observed variation. The estimates of mean (m) as well as additive (d) and dominance (h) effects were significant, and the dominance effect was greater than the additive effect (Table 4). The large and negative dominance effect indicated that leaf resistance was predominantly controlled by nonadditive genetic effects with recessive alleles for leaf resistance in PI 270545, hence the lowest positive degree of dominance.

Table 4.

A, B, and C scaling test and estimates of components in a generation means analysis for leaf and stem resistance to powdery mildew in PI 270545 × PI 269677.

Table 4.

The large dominance effect suggests that selection of resistant plants should be done after self-pollination to identify the resistant recessive genotypes. Recurrent selection can also be useful, because it increases the frequency of resistant alleles for leaf resistance in the population. Failure to detect nonallelic interaction in leaf rating, as inferred from nonsignificance of the epistatic effects (Table 4), may arise from an unequal dispersion of genes with similar effects between the two parents. Judging from the mean value of F2, it is likely that genes for powdery mildew susceptibility are not only in the susceptible parent, but also present in the moderately resistant parent. The negative dominance effect in leaf rating indicates that, in PI 270545, the high resistance gene is recessive, whereas the moderate resistance gene is dominant. Significant additive (0.90) and dominance (–4.34) effects explained 7% and 67% of the variation in leaf rating, respectively (Table 4). The remaining variation may be contributed by undetected nonallelic effects. This agrees with the high narrow-sense heritability of 71%, indicating that improvement in leaf resistance can be achieved through selection. Application of QTL mapping analysis may contribute to the detection of epistatic effects in this population. Zalapa et al. (2007) reported detection of digenic epistatic effects in melon architectural traits using QTL analysis.

Stem resistance.

In contrast to leaf resistance, nonsignificance of the ABC components was supported by the joint scaling test. The additive-dominance model was adequate in explaining the variation in stem rating [ 1.98; P = 0.6]. Both additive (d) and dominance (h) effects were significant, but the additive effect was negative and considerably larger than the dominance effect, indicating that stem resistance was predominantly controlled by additive effects. Because larger additive effects were important for stem resistance, breeding progress would be faster than for leaf resistance.

The i, j, and l effects were not significant, demonstrating absence of a nonallelic interaction. The contribution of additive and dominance effects was 58% and 15%, respectively. A high heritability (79%) indicates that selection for stem resistance in this population would be effective.

Conclusions

Powdery mildew resistance in watermelon PI 270545 was controlled by a recessive gene for high resistance and a dominant gene for moderate resistance. Based on generation means analysis, the dominance genetic effect was larger for leaf resistance, whereas the additive genetic effect was larger for stem resistance. The large narrow-sense heritability in PI 269677 × PI 270545 combined with major additive genetic effects suggested that selecting for powdery mildew stem resistance in the segregating population of this cross could be done efficiently using single-plant selection, whereas for leaf resistance, selection in self-pollinated progeny rows would be necessary.

Literature Cited

  • CarsonM.L.HookerA.L.1981Inheritance of resistance to stalk rot of corn caused by Colletotrichum graminicolaPhytopathology7111901196

  • CavalliL.L.1952Analysis of linkage in quantitative inheritance p. 135–144. In: Rieve E.C. and C.W. Waddington (eds.). Quantitative inheritance. HMSO London UK

  • CrowJ.F.KimuraM.1970An introduction to population genetics. Burgess Minneapolis MN

  • DavisA.R.BrutonB.D.PairS.D.ThomasC.E.2001Powdery mildew: An emerging disease of watermelon in the United StatesCucurbit Genet. Coop. Rep.244248

    • Search Google Scholar
    • Export Citation
  • DavisA.R.LeviA.TettehA.Y.WehnerT.C.RussoV.PitratM.2007Evaluation of watermelon and related species for resistance to race 1W powdery mildewJ. Amer. Soc. Hort. Sci.132790795

    • Search Google Scholar
    • Export Citation
  • DavisA.R.WehnerT.C.LeviA.KingS.R.2005Update on powdery mildew resistance screening in watermelonHortScience40871[Abstract]

  • EpinatC.PitratM.BertrandF.1993Genetic analysis of resistance of five melon lines to powdery mildewsEuphytica65135144

  • FengD.X.1996The recent progress in resistance powdery mildew breeding of CucurbitaceousChina Vegetable75559[in Chinese with English abstract]

    • Search Google Scholar
    • Export Citation
  • IqbalM.Z.NadeemM.A.2003Generation mean analysis for seed cotton yield and number of sympodial branches per plant in cotton (Gossypium hirsutum, L.)Asian J. Plant Sci.2395399

    • Search Google Scholar
    • Export Citation
  • JungM.WeldekidanT.SchaffD.PatersonA.TingeyS.HawkJ.1994Generation-means analysis and quantitative trait locus mapping of anthracnose stalk rot genes in maizeTheor. Appl. Genet.89413418

    • Search Google Scholar
    • Export Citation
  • KenigsbuchD.CohenY.1992Inheritance and allelism of genes for resistance to races 1 and 2 of Sphaerotheca fuliginea in muskmelonPlant Dis.76626629

    • Search Google Scholar
    • Export Citation
  • MatherK.1949Biometrical genetics. Mather and Co. London UK

  • MatherK.JinksJ.L.1971Biometrical genetics: The study of continuous variation. Cornell University Press Ithaca NY

  • McCreightJ.D.2003Genes for resistance to powdery mildew races 1 and 2 U.S. in melon PI 313970HortScience38591594

  • McCreightJ.D.PitratM.ThomasC.E.KinshasaA.N.BohnG.W.1987Powdery mildew resistance genes in muskmelonJ. Amer. Soc. Hort. Sci.112156160

    • Search Google Scholar
    • Export Citation
  • McGrathM.T.2001Distribution of cucurbit powdery mildew races 1 and 2 on watermelon and muskmelonPhytopathology91197[Abstract]

  • McGrathM.T.ThomasC.E.1996Powdery mildew p. 28-30. In: T.A. Zitter D.L. Hopkins and C.E. Thomas (eds.). Compendium of cucurbit diseases. The American Phytopathological Society St. Paul MN

  • PerchepiedL.BardinM.DogimontC.PitratM.2005Relationship between loci conferring downy mildew and powdery mildew resistance in melon assessed by quantitative trait loci mappingPhytopathology95556565

    • Search Google Scholar
    • Export Citation
  • PitratM.DogimontC.BardinM.1998Resistance to fungal diseases of foliage in melon p. 167–173. In: McCreight J.D. (ed.). Cucurbitaceae 98. Evaluation and enhancement of cucurbits germplasm. American Society for Horticultural Science Pacific Grove CA

  • RobinsonR.W.ProvvidentiR.ShailJ.W.1975Inheritance of susceptibility to powdery mildew in the watermelonJ. Hered.66310311

  • SaudhuB.S.NittalV.P.1988Genetic analysis of yield and its components in Desi cottonInd. J. Agr. Res.22105109

  • TettehA.Y.WehnerT.C.DavisA.R.2010Identifying resistance to powdery mildew race 2W in the USDA-ARS Watermelon Germplasm CollectionCrop Sci.50933939

    • Search Google Scholar
    • Export Citation
  • TettehA.Y.WehnerT.C.DavisA.R.2013Inheritance of resistance to the new race of powdery mildew in watermelonCrop Sci.53880887

  • TomasonY.GibsonP.T.2006Fungal characteristics and varietal reaction of powdery mildew species on Cucurbits in the steppes of UkraineAgron. Res.4549562

    • Search Google Scholar
    • Export Citation
  • WarnerJ.N.1952A method for estimating heritabilityAgron. J.44427430

  • ZalapaJ.E.StaubJ.E.McCreightJ.D.ChungS.M.CuevasH.2007Detection of QTL for yield-related traits using recombinant inbred lines derived from exotic and elite US Western Shipping melon germplasmTheor. Appl. Genet.11411851201

    • Search Google Scholar
    • Export Citation
  • ZhangH.GuoS.GongG.RenY.DavisA.R.YongX.2011Sources of resistance to race 2WF powdery mildew in U.S. watermelon plant introductionsHortScience4613491352

    • Search Google Scholar
    • Export Citation

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Contributor Notes

This work was supported in part by the graduate school assistantship provided by North Carolina State University, the North Carolina Agricultural Research Service, the Ghana Government Scholarship Fund, and the American Association of University Women.

We thank Tammy L. Ellington and Allen Gordon for technical assistance.

Previously with U.S. Department of Agriculture, Agriculture Research Service, South Central Agriculture Research Laboratory, Lane, OK 74555.

To whom reprint requests should be addressed; e-mail todd_wehner@ncsu.edu.

Article Sections

Article References

  • CarsonM.L.HookerA.L.1981Inheritance of resistance to stalk rot of corn caused by Colletotrichum graminicolaPhytopathology7111901196

  • CavalliL.L.1952Analysis of linkage in quantitative inheritance p. 135–144. In: Rieve E.C. and C.W. Waddington (eds.). Quantitative inheritance. HMSO London UK

  • CrowJ.F.KimuraM.1970An introduction to population genetics. Burgess Minneapolis MN

  • DavisA.R.BrutonB.D.PairS.D.ThomasC.E.2001Powdery mildew: An emerging disease of watermelon in the United StatesCucurbit Genet. Coop. Rep.244248

    • Search Google Scholar
    • Export Citation
  • DavisA.R.LeviA.TettehA.Y.WehnerT.C.RussoV.PitratM.2007Evaluation of watermelon and related species for resistance to race 1W powdery mildewJ. Amer. Soc. Hort. Sci.132790795

    • Search Google Scholar
    • Export Citation
  • DavisA.R.WehnerT.C.LeviA.KingS.R.2005Update on powdery mildew resistance screening in watermelonHortScience40871[Abstract]

  • EpinatC.PitratM.BertrandF.1993Genetic analysis of resistance of five melon lines to powdery mildewsEuphytica65135144

  • FengD.X.1996The recent progress in resistance powdery mildew breeding of CucurbitaceousChina Vegetable75559[in Chinese with English abstract]

    • Search Google Scholar
    • Export Citation
  • IqbalM.Z.NadeemM.A.2003Generation mean analysis for seed cotton yield and number of sympodial branches per plant in cotton (Gossypium hirsutum, L.)Asian J. Plant Sci.2395399

    • Search Google Scholar
    • Export Citation
  • JungM.WeldekidanT.SchaffD.PatersonA.TingeyS.HawkJ.1994Generation-means analysis and quantitative trait locus mapping of anthracnose stalk rot genes in maizeTheor. Appl. Genet.89413418

    • Search Google Scholar
    • Export Citation
  • KenigsbuchD.CohenY.1992Inheritance and allelism of genes for resistance to races 1 and 2 of Sphaerotheca fuliginea in muskmelonPlant Dis.76626629

    • Search Google Scholar
    • Export Citation
  • MatherK.1949Biometrical genetics. Mather and Co. London UK

  • MatherK.JinksJ.L.1971Biometrical genetics: The study of continuous variation. Cornell University Press Ithaca NY

  • McCreightJ.D.2003Genes for resistance to powdery mildew races 1 and 2 U.S. in melon PI 313970HortScience38591594

  • McCreightJ.D.PitratM.ThomasC.E.KinshasaA.N.BohnG.W.1987Powdery mildew resistance genes in muskmelonJ. Amer. Soc. Hort. Sci.112156160

    • Search Google Scholar
    • Export Citation
  • McGrathM.T.2001Distribution of cucurbit powdery mildew races 1 and 2 on watermelon and muskmelonPhytopathology91197[Abstract]

  • McGrathM.T.ThomasC.E.1996Powdery mildew p. 28-30. In: T.A. Zitter D.L. Hopkins and C.E. Thomas (eds.). Compendium of cucurbit diseases. The American Phytopathological Society St. Paul MN

  • PerchepiedL.BardinM.DogimontC.PitratM.2005Relationship between loci conferring downy mildew and powdery mildew resistance in melon assessed by quantitative trait loci mappingPhytopathology95556565

    • Search Google Scholar
    • Export Citation
  • PitratM.DogimontC.BardinM.1998Resistance to fungal diseases of foliage in melon p. 167–173. In: McCreight J.D. (ed.). Cucurbitaceae 98. Evaluation and enhancement of cucurbits germplasm. American Society for Horticultural Science Pacific Grove CA

  • RobinsonR.W.ProvvidentiR.ShailJ.W.1975Inheritance of susceptibility to powdery mildew in the watermelonJ. Hered.66310311

  • SaudhuB.S.NittalV.P.1988Genetic analysis of yield and its components in Desi cottonInd. J. Agr. Res.22105109

  • TettehA.Y.WehnerT.C.DavisA.R.2010Identifying resistance to powdery mildew race 2W in the USDA-ARS Watermelon Germplasm CollectionCrop Sci.50933939

    • Search Google Scholar
    • Export Citation
  • TettehA.Y.WehnerT.C.DavisA.R.2013Inheritance of resistance to the new race of powdery mildew in watermelonCrop Sci.53880887

  • TomasonY.GibsonP.T.2006Fungal characteristics and varietal reaction of powdery mildew species on Cucurbits in the steppes of UkraineAgron. Res.4549562

    • Search Google Scholar
    • Export Citation
  • WarnerJ.N.1952A method for estimating heritabilityAgron. J.44427430

  • ZalapaJ.E.StaubJ.E.McCreightJ.D.ChungS.M.CuevasH.2007Detection of QTL for yield-related traits using recombinant inbred lines derived from exotic and elite US Western Shipping melon germplasmTheor. Appl. Genet.11411851201

    • Search Google Scholar
    • Export Citation
  • ZhangH.GuoS.GongG.RenY.DavisA.R.YongX.2011Sources of resistance to race 2WF powdery mildew in U.S. watermelon plant introductionsHortScience4613491352

    • Search Google Scholar
    • Export Citation

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