Review of Watermelon Genetics for Plant Breeders

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Review of Watermelon Genetics for Plant Breeders
Gabriele Gusmini and Todd C. Wehner

Department of Horticultural Science, North Carolina State University, Raleigh, NC 27695-7609

In watermelon [Citrullus lanatus (Thunb.) Matsum. & Nakai var. lanatus] breeding, most of the useful traits subject to improvement or study have been either fruit characteristics or resistance to diseases of abiotic and biotic origin, often controlled by single genes. The genetics of watermelon have been studied extensively, and many genes have been characterized during the last 60 to 70 years (8, 9, 14, 15, 40).

Genetics of Plant Architecture and Sex Expression

Plant architecture traits have been minor objectives for watermelon breeders, often limited to the development of cultivars with short vines (dwarf type) to be used by home gardeners. The inheritance of dwarfism has been studied, and some genes producing the dwarf phenotype have been described (19, 23, 25). The dwarf type can be obtained using one of the four genes: dw–1, dw–2, dw–3, and ms-dw. Dwarfism in watermelon is caused by shortened internodes (dw–1) or reduced internode number (dw–2). The mechanism of action of the dw-3 allele has not been reported.
Genes regulating sex expression in watermelon have not been described, with the exception of the a gene for andromonoecious plants, the dominant allele producing monoecious (A) (42). No gynoecious or parthenocarpic germplasm has been identified in watermelon, as opposed to cucumber (Cucumis sativus L.), where seedless fruit can be obtained from a gynoecious, parthenocarpic cultivar grown in isolation from cucumber pollen. Thus, seedless watermelons are produced only on sterile triploid plants, by inducing fruit formation with diploid pollen.
Male-sterility has been reported in several mutant lines, and four genes have been described to confer this trait. The ms (ms-1) gene causes the development of small anthers and pollen abortion (59, 60). In addition, the ms-2 and ms-dw genes for male sterility have recently been identified. The gms gene, instead, induces male sterility due to chromosome desynapsis, accompanied by absence of trichomes on the leaves (glabrous male sterile) (53, 54). Technological application of these two genes has been pursued for the production of hybrid seed, even though hand-pollination and daily removal of male flowers are still the most common techniques, probably due to the low cost of labor in the countries of seed production (Asia and Central America) (24).

Genetics of Resistance

Little information is available on the genetics of resistance to abiotic stresses in watermelon, even though traits such as drought and heat tolerance would be useful traits. A single dominant gene (Ctr) was identified for tolerance of cold temperatures (<20°C at night) at the seedling stage (37, 38).
The primary nematode species attacking watermelon are the peanut [Meloidogyne arenaria (Neal) Chitw.], southern [M. incognita, (Kofoid and White) Chitw.], and Javanese [M. javanica (Treub) Chitw.] root-knot nematodes. Although losses to these parasites may be as much as 50% (24), the extensive use of fumigants has delayed the search for nematode resistant germplasm and the study of the genetics of resistance. Currently, as methyl bromide is phased out, interest is increasing in the development of nematode resistant cultivars.
Genetic resistance to insect pests does not have a very important role in the protection of watermelon crops. So far, insect control is mostly achieved chemically. Nevertheless, genes for resistance to the red pumpkin beetle (Aulacophora foveicollis Lucas), Af, and to the fruit fly (Dacus cucurbitae Coquillett), Fwr, have been identified. Resistance for both genes, Af and Fwr, was dominant to susceptibility (21, 51). Most insect pests in the United States are specific to each region of watermelon production, making it economically less advantageous to develop insect resistant cultivars. Nevertheless, some pests are common over different areas, i.e. the melon aphid (Aphis gossypii Glover) and the cucumber beetle species Acalymma vittatum Fabricius and Diabrotica undecimpunctata howardi Barber (24). In those cases, genetic resistance may be an efficient alternative to chemical control.
Various species of fungi, viruses, and bacteria cause destructive diseases of watermelon. In the United States, fungal diseases are a major limitation on the watermelon industry in the Southeastern region, while viruses are more damaging in Western production areas. The most important fungal diseases (with causal agent) are anthracnose (Colletotrichum lagenarium (Pass.) Ellis & Halst), downy mildew (Pseudoperonospora cubensis Berk. & M.A. Curtis), Fusarium wilt (Fusarium oxysporum Schlechtend.:Fr. f. sp. niveum (E.F. Sm.) W.C. Snyder & H.N. Hans), gummy stem blight (Didymella bryoniae (Auersw.) Rehm), Monosporascus root rot and vine decline (Monosporascus cannonballus Pollack & Uecker), Phytophthora blight (Phytophthora capsici Leonian), Pythium damping-off (Pythium spp.), and powdery mildew (Podosphaera xanthii (Castagne) U. Braun & N. Shishkoff). The main viral diseases are cucumber mosaic (CMV), papaya ringspot (PRSV type W, previously known as WMV), watermelon mosaic (WMV; previously known as WMV-2), squash mosaic (SqMV), zucchini yellow mosaic (ZYMV), and the watermelon vine decline virus. Bacterial fruit blotch, caused by Acidovorax avenae subsp. citrulli Schaad et al. is a serious disease that is seedborne. Despite the high number of biotic pathogens listed, the genetics of resistance have been described only for the control of Fusarium wilt, gummy stem blight, anthracnose, watermelon mosaic, and zucchini yellow mosaic (11, 57).
Seven races of anthracnose have been reported, but races 1, 2, and 3 appear to be the most important in watermelon (24). Most cultivars are resistant to races 1 and 3, and resistance sources to race 2 have been identified, with PI 512385 being the most resistant (3). Resistance to all three races was inherited as a dominant gene in multiple crosses: Ar-1 conferred resistance to races 1 and 3 (22), and Ar-21 to race 2 (56).
Resistance has been found for three races (0, 1, and 2) of Fusarium wilt, and watermelon differentials have been identified. 'Black Diamond' and 'Sugar Baby' are susceptible to all races, 'Quetzali' and 'Mickylee' are resistant to race 0, 'Charleston Gray' is resistant to race 0 and moderately resistant to race 1, 'Calhoun Gray' is resistant to races 0 and 1, and PI 296341 and PI 271769 are resistant to all races (Table 1) (24). In addition, the inheritance of resistance to race 1 has been described. Resistance was inherited as a single dominant gene (Fo-1) in crosses of the resistant 'Calhoun Gray' or 'Summit' with the susceptible 'NH Midget' (16).
Resistance to gummy stem blight was found in PI 189225 and PI 271778 and deployed as a single recessive gene (db) to develop the resistant cultivars 'AU-Producer', 'AU-Golden Producer', 'AU-Jubilant', and 'AU-Sweet Scarlet' (28-31). Nevertheless, these cultivars were less resistant than their resistant parents, thus demonstrating the difficulty of transferring resistance to gummy stem blight.
Watermelon resistance to viruses has been identified for PRSV, WMV, and ZYMV (24). So far, two genes for resistance to zucchini yellow mosaic have been reported. Plants homozygous for zym-FL were resistant to a strain of ZYMV from Florida (36). More recently, resistance to a Chinese strain of the same virus was inherited as the single recessive gene zym-CH (57). In addition, Xu et al. (2004) estimated that tolerance to watermelon mosaic in two crosses was controlled by a minimum of two genes with high broad-sense heritability.
Finally, one recessive gene (pm) for the susceptibility to powdery mildew was reported (41). In addition, resistance to the isolates causing problems now has been reported, and research is in progress on the inheritance of resistance to this important new disease in watermelon.

Genetics of Fruit Characteristics

The watermelon fruit consists of the exocarp, mesocarp, and endocarp. The endocarp is the seed-containing part that is consumed as food, and the mesocarp (white crisp inner layer) and exocarp (thin green outer layer) are usually referred to as the rind. Fruit traits of interest in watermelon can be grouped into six categories: 1) yield, 2) shape, 3) weight, 4) rind, 5) flesh, and 6) seeds. Each of these categories includes characteristics that are important for successful cultivars. Yield may be determined by the number of fruit per unit of production and may be separated into marketable and non-marketable yield (culls), based on the overall external appearance of the fruit. The rind may differ in color, pattern, thickness, toughness, and flexibility. The flesh may differ in color, texture, sweetness (sugar or total soluble solids content), and resistance to hollowheart (internal voids). The seeds may differ for color, size, and resistance to formation of hard seed coats in triploid (seedless) watermelons.
The inheritance of yield components in watermelon was studied extensively in the 1960s and 1970s. Heterosis and general (GCA) and specific (SCA) combining ability were measured in many crosses (6, 7, 26, 27, 46-49). More recent studies of the effects of reciprocal crosses on yield components in watermelon have been contradictory (10, 39, 43). Heterosis was inconsistent over experiments, but the studies involved either diallel or top crosses of elite inbreds, and not a random set of lines from a population. Furthermore, the experiments included only a small number of non-randomly chosen elite cultivars as parents, so the results are valid only for those specific crosses and are not generally applicable.
Watermelon fruit can be round, oval, blocky, or elongate in shape (24). The inheritance of fruit shape has not been widely studied, but the round, oval, and elongate phenotypes were shown to be determined by the incomplete dominance of the O gene. The homozygous dominant plants had elongated fruit, the homozygous recessive fruit were round (spherical), and the heterozygous fruit were oval (33, 55). In addition, the shape of the fruit can be predicted by the shape of the ovary at anthesis, thus making ovary shape a useful marker for things such as hybrid seed production (52).
The fruit of the cultivated watermelon may vary in weight from 1 to 100 kg. In the United States, commercial fruit are usually classified into four categories: icebox (<5.5 kg), small or pee-wee (5.5-8.0 kg), medium (8.1-11.0 kg), large (11.1-14.5 kg), and giant (>14.5 kg) (24). Recently, the icebox category was divided into mini (<4 kg) and icebox (4-5.5 kg) fruit sizes. Fruit weight in watermelon production is a yield component, which contributes to total yield per unit of land. However, since fruit of different sizes are marketed in different categories, fruit weight should be regarded as a descriptor of fruit type. In two preliminary studies of inheritance of fruit weight, significant additive, dominant, and epistatic effects were reported, dominance and dominance-by-dominance being the largest gene effects (4, 44). Nevertheless, single genes or quantitative trait loci have not been identified for the weight of watermelon fruit.
Both mechanical characteristics and color of the watermelon rind are of great importance to the development of cultivars with good shipping ability, long shelf-life, and attractive appearance. The only gene reported to influence the mechanical characteristics of the rind (toughness and flexibility) was the t gene for the thin, tender rind, bursting when cut, from 'California Klondike' (35), renamed e for explosive rind by Poole (1944). So far, no study has described the inheritance of rind toughness among watermelon families with non-explosive rind.
The inheritance of rind color and pattern has been studied since the 1930s. The most common rind colors are solid green (dark, medium, and light), striped (narrow, medium, and wide dark green stripes on a light green background), and gray (medium green lines on a light green background). The genes described for the different skin colors and patterns are part of a three-allele series at the g locus: G for dark green, gs for striped, and g for light green (55). However, this model does not seem to apply in all watermelon cultivars. Furthermore, the inheritance of some rind colors such as gray or medium-green have not been published, even though these have been two common colors during the last century of watermelon breeding.
The genetics of the flesh color in watermelon have been studied and genes for the red, orange, salmon yellow, canary yellow, and white colors have been reported. A triple-allelic series was identified at the y locus to regulate red, orange, and salmon yellow flesh colors (Y, yo, and y, respectively) (17, 18, 32, 35). The canary yellow color (C gene) was dominant to pink (c) and epistatic to red (Y) (18, 32). In addition, the red color was also recorded in individuals homozygous for C, where the production of the yellow pigment was inhibited by the i-C gene (inhibitor of canary yellow) (18, 40). A third gene for the yellow flesh (B) has also been described in a breeding line. The white flesh gene (Wf) was epistatic to B (15, 45). Nevertheless, breeding for specific flesh colors has often been challenging, due to frequent distortion of the inheritance of some of these genes, thus suggesting that a more complex model may determine flesh color in segregating populations of watermelon.
Sugar content of the flesh in watermelon is measured as total soluble solids (degrees Brix). It is the major component of taste, and may vary from 1 to 16° Brix (24). So far, no study of the genetics of total soluble solids based on a set of cultivars representative of a large range of watermelon germplasm has been reported. Furthermore, preliminary studies included parents that differed by only 2 to 3 °Brix in sugar content (2, 5). A study of crosses between cultivars at the extremes of the range of watermelon sweetness would be useful to the improvement of the organoleptic properties of the flesh of watermelon.

Genetics of Seed Characteristics

Watermelon seeds usually are classified according to their color and size, both traits being of great interest to breeders. Seed color may affect the appearance of cut fruit greatly (seed color that contrasts with flesh color are usually preferred), while their size can limit the edibility of the fruit itself. Large seeds usually are removed from the flesh when consumed, while tiny (tomato seed) seeds might be ingested. Most of the current commercial cultivars have short (small) or medium size seeds, rather than long (large) or tomato seed.
Commercially, watermelon seeds are categorized by size: long (or large), medium, short (or small) (approximately 10, 7, and 5 mm long), and tomato seed (watermelon seeds the size of tomato seeds). According to Poole et al. (1941), the l and s genes interact to determine seed size for the long, medium, and short classes (ll SS for long, LL SS for medium, and LL ss or ll ss for short). The tomato seed size was studied in a cross between a 'Sugar Baby' mutant with tomato seed size and 'GN-1', with short seeds. The tomato seed size trait was inherited as a single recessive gene (ts) (58). The interaction of ts with l and s has not been described so far. In addition, a gene (Ti), dominant over medium seeds, has been described for the so-called "tiny" seed-size in 'Sweet Princess' (50). Tiny seeds have size similar to small seeds (Fig. 2).
The main colors of watermelon seeds are white, tan, brown, black, red, green, and dotted (24). In addition, seeds may have lighter or darker margins (ring), or may be covered by an additional layer of fleshy pericarp in Egusi cultivars, as controlled by the eg gene (Fig. 1) (12, 13).
The genes r, t, and w determine seed color. Black is given by triple dominant; mottled is homozygous recessive only for w; tan is homozygous recessive only for t; white with tan tip is homozygous recessive only for t and w; red is homozygous recessive only for r and t. Finally, triple recessive results in white seeds with pink tip (34). The dotted (renamed from mottled) seed type is determined by the d gene, acting as a modifier of black: RR TT WW DD gives solid black and RR TT WW dd gives dotted black seed-coat (20, 32, 34).
Seeds of certain cultivars show vertical cracks (parallel to the longest axis of the seed) of the seed-coat, usually less than one mm wide and about 50-75% of the seed length. The development of these cracks has been determined to be under the genetic control of cr (1). It is not known if this phenotype has any advantage in germination and whether growers would perceive seeds with cracks as defective, compared to normal seeds.
Other genes of minor interest to breeders have been studied and described, as reported in the current watermelon gene list (11). These include genes for green flower color (gf), golden leaf color (go), along with several genes coding for specific proteins. In addition, watermelon breeders have selected for many different characteristics, such as flesh color, rind pattern, plant architecture, and leaf shape, for which the inheritance is unknown so far. Efforts are under way to collect mutants for storage and distribution by the Cucurbit Genetics Cooperative watermelon gene curators (T.C. Wehner and S.R. King).
Literature Cited

  1. Abd el Hafez, A. A., A. K. Gaafer, and A. M. M. Allam. 1981. Inheritance of flesh colour, seed coat cracks and total soluble solids in watermelon and their genetic relations. I. Quantitative traits. Acta Agronomica Academiae Scientiarum Hungaricae 30:82-86.

  2. Abd el Hafez, A. A., A. K. Gaafer, and A. M. M. Allam. 1985. Inheritance of flesh colour, seed coat cracks and total soluble solids in watermelon and their genetic relations. II. Quantitative characters and the association between various characters. Acta Agronomica Academiae Scientiarum Hungaricae 34:84-89.

  3. Boyhan, G., J. D. Norton, and B. R. Abrahams. 1994. Screening for resistance to anthracnose (race 2), gummy stem blight, and root knot nematode in watermelon germplasm. Cucurbit Genetics Cooperative Report 17:106-110.

  4. Brar, J. S., and K. S. Nandpuri. 1974. Inheritance of fruit weight in water-melon [Citrullus lanatus (Thunb.) Mansf.]. Journal of Research, Punjab Agricultural Service 11:140-144.

  5. Brar, J. S., and K. S. Nandpuri. 1977. A note on the inheritance of total soluble solids in watermelon (Citrullus lanatus (Thunb) Mansf.). Haryana Journal of Horticultural Sciences 6:193-195.

  6. Brar, J. S., and A. S. Sidhu. 1977. Heterosis and combining ability of earliness and quality characters in watermelon (Citrullus lanatus (Thunb. Mansf.). II. Journal of Research 14:272-278.

  7. Brar, J. S., and B. S. Sukhija. 1977. Line x tester analysis of combining ability in watermelon [Citrullus lanatus (Thunb) Mansf]. Indian Journal of Horticulture 34:410-414.

  8. Cucurbit Gene List Committee. 1979. New genes for the Cucurbitaceae. Cucurbit Genetics Cooperative Report 2:49-53.

  9. Cucurbit Gene List Committee. 1982. Update of cucurbit gene list and nomenclature rules. Cucurbit Genetics Cooperative Report 5:62-66.

  10. Gill, B. S., and J. C. Kumar. 1988. Combining ability analysis in watermelon (Citrullus lanatus Thunb. Mansf.). Indian Journal of Horticulture 45:104-109.

  11. Guner, N., and T. C. Wehner. 2003. Gene list for watermelon. Cucurbit Genetics Cooperative Report 26:76-92.

  12. Gusmini, G., R. L. Jarret, and T. C. Wehner. 2004. Inheritance of 'Egusi' seed-type in watermelon (Citrullus lanatus var. lanatus). Journal of Heredity 95:268-270.

  13. Gusmini, G., and T. C. Wehner, All about watermelon - Egusi. 2003.

  14. Henderson, W. R. 1991. Gene list for watermelon. Cucurbit Genetics Cooperative Report 14:129-138.

  15. Henderson, W. R. 1992. Corrigenda to 1991 watermelon gene list (CGC 14:129-137). Cucurbit Genetics Cooperative Report 15:110.

  16. Henderson, W. R., S. F. Jenkins, and J. O. Rawlings. 1970. The inheritance of Fusarium wilt resistance in watermelon, Citrullus lanatus (Thunb.) Mansf. Proceedings of American Society for Horticultural Science 95:276-282.

  17. Henderson, W. R., G. H. Scott, and T. C. Wehner. 1989. Inheritance of orange flesh color in watermelon. Cucurbit Genetics Cooperative Report 12:59-63.

  18. Henderson, W. R., G. H. Scott, and T. C. Wehner. 1998. Interaction of flesh color genes in watermelon. Journal of Heredity 89:50-53.

  19. Huang, H., X. Zhang, Z. Wei, Q. Li, and X. Li. 1998. Inheritance of male-sterility and dwarfism in watermelon [Citrullus lanatus (Thunb.) Matsum. and Nakai]. Scientia Horticulturae 74:175-181.

  20. Kanda, T. 1951. The inheritance of seed-coat colouring in the watermelon. Japanese Journal of Genetics 7:30-48.

  21. Khandelwal, R. C., and P. Nath. 1978. Inheritance of resistance to fruit fly in watermelon. Canadian Journal of Genetics and Cytology 20:31-34.

  22. Layton, D. V. 1937. The parasitism of Colletotrichum lagenarium (Pass.) Ells. and Halst. Iowa Agricultural Experimental Station Annual Bulletin 223:37-67.

  23. Liu, P. B. W., and J. B. Loy. 1972. Inheritance and morphology of two dwarf mutants in watermelon. Journal of American Society for Horticultural Science 97:745-748.

  24. Maynard, D. N., ed. 2001. Watermelons. Characteristics, production, and marketing. I ed., Alexandria, Virginia: ASHS Press. 227 pp.

  25. Mohr, H. C., and M. S. Sandhu. 1975. Inheritance and morphological traits of a double recessive dwarf in watermelon, Citrullus lanatus (Thunb.) Mansf. Journal of American Society for Horticultural Science 100:135-137.

  26. Nandpuri, K. S., J. C. Kumar, and G. S. Dhillon. 1974. Heterosis in watermelon. The Punjab Horticultural Journal 14:75-83.

  27. Nandpuri, K. S., J. C. Kumar, and G. S. Dhillon. 1975. Combining ability estimates in a set of top crosses in watermelon (Citrullus lanatus Sch.). The Punjab Horticultural Journal 15:65-70.

  28. Norton, J. D. 1979. Inheritance of resistance to gummy stem blight caused by Didymella bryoniae in watermelon. HortScience 14:630-632.

  29. Norton, J. D., G. Boyhan, D. A. Smith, and B. R. Abrahams. 1993. 'AU-Golden Producer' watermelon. HortScience 28:681-682.

  30. Norton, J. D., G. Boyhan, D. A. Smith, and B. R. Abrahams. 1995. 'AU-Sweet Scarlet' watermelon. HortScience 30:393-394.

  31. Norton, J. D., R. D. Cosper, D. A. Smith, and K. S. Rymal. 1986. 'AU-Jubilant' and 'AU-Producer' watermelons. HortScience 21:1460-1461.

  32. Poole, C. F. 1944. Genetics of cultivated cucurbits. Journal of Heredity 35:122-128.

  33. Poole, C. F., and P. C. Grimball. 1945. Interaction of sex, shape, and weight genes in watermelon. Journal of Agricultural Research, U.S. 71:533-552.

  34. Poole, C. F., P. C. Grimball, and D. R. Porter. 1941. Inheritance of seed characters in watermelon. Journal of Agricultural Research, U.S. 63:433-456.

  35. Porter, D. R. 1937. Inheritance of certain fruit and seed characters in watermelons. Hilgardia 10:489-509.

  36. Provvidenti, R. 1991. Inheritance of resistance to the Florida strain of zucchini yellow mosaic virus in watermelon. HortScience 26:407-408.

  37. Provvidenti, R. 1992. Cold resistance in accessions of watermelon from Zimbabwe. Cucurbit Genetics Cooperative Report 15:67-68.

  38. Provvidenti, R. 2003. Naming the gene conferring resistance to cool temperatures in watermelon. Cucurbit Genetics Cooperative Report 26:31.

  39. Rajendran, P. C., and S. Thamburaj. 1993. Heterosis in watermelon (Citrullus lanatus Thunb. Mansf.). The Madras Agricultural Journal 80:40-46.

  40. Rhodes, B., and F. Dane. 1999. Gene list for watermelon. Cucurbit Genetics Cooperative Report 22:61-77.

  41. Robinson, R. W., R. Provvidenti, and J. W. Shail. 1975. Inheritance of susceptibility to powdery mildew in the watermelon. Journal of Heredity 66:310-311.

  42. Rosa, J. T. 1928. The inheritance of flower types in Cucumis and Citrullus. Hilgardia 3:233-250.

  43. Sachan, S. C. P., and P. Nath. 1976. Combining ability of some quantitative characters in 10 x 10 diallel crosses of watermelon, Citrullus lanatus (Thunb.) Mansf. Egyptian Journal of Genetics and Cytology 5:65-79.

  44. Sharma, R. R., and B. Choudhury. 1988. Studies on some quantitative characters in watermelon (Citrullus lanatus Thunb. Mansf.). I. Inheritance of earliness and fruit weight. Indian Journal of Horticulture 45:80-84.

  45. Shimotsuma, M. 1963. Cytogenetical studies in the genus Citrullus. VII. Inheritance of several characters in watermelon. Japanese Journal of Breeding 13:235-240.

  46. Sidhu, A. S., and J. S. Brar. 1977. Heterosis and combining ability of yield and its components in watermelon (Citrullus lanatus (Thunb.) Mansf.). Journal of Research 14:52-58.

  47. Sidhu, A. S., and J. S. Brar. 1985. Genetic divergence and hybrid performance in watermelon. Indian Journal of Agricultural Sciences 55:459-461.

  48. Sidhu, A. S., J. S. Brar, and S. P. S. Gill. 1977. Mode of inheritance and gene action for yield and its components in watermelon (Citrullus lanatus (Thumb) Mansf). Journal of Research of Punjab Agriculture University 14:419-422.

  49. Sidhu, A. S., J. S. Brar, and S. P. S. Gill. 1977. Mode of inheritance of earliness and quality characters in watermelon (Citrullus lanatus (Thumb) Mansf). Journal of Research of Punjab Agriculture University 14:423-426.

  50. Tanaka, T., S. Wimol, and T. Mizutani. 1995. Inheritance of fruit shape and seed size of watermelon. Journal of Japanese Society for Horticultural Science 64:543-548.

  51. Vashistha, R. N., and B. Choudhury. 1972. Inheritance of resistance to red punpkin beetle in muskmelon, bottle gourd and watermelon. Proceedings of 3rd International Symposium on Sub-Tropical and Tropical Horticulture:75-81.

  52. Warid, A., and A. A. Abd el Hafez. 1976. Inheritance of marker genes of leaf color and ovary shape in watermelon. The Lybian Journal of Science 6:1-8.

  53. Watts, W. M. 1962. A marked male-sterile mutant in watermelon. Proceedings of American Society for Horticultural Science 81:498-505.

  54. Watts, W. M. 1967. Development of disease resistance and seed production in watermelon stocks carrying the msg gene. Proceedings of American Society for Horticultural Science 91:579-583.

  55. Weetman, L. M. 1937. Inheritance and correlation of shape, size and color in the watermelon, Citrullus vulgaris Schrad. Iowa Agricultural Experimental Station Annual Bulletin 228:224-256.

  56. Winstead, N. N., M. J. Goode, and W. S. Barham. 1959. Resistance in watermelon

to Colletotrichum lagenarium races 1, 2, and 3. Plant Disease Reporter 43:570-577.

  1. Xu, Y., D. Kang, Z. Shi, H. Shen, and T. C. Wehner. 2004. Inheritance of resistance to zucchini yellow mosaic virus in watermelon. Journal of Heredity 95:498-502.

  2. Zhang, J. N. 1996. Inheritance of seed size from diverse crosses in watermelon. Cucurbit Genetics Cooperative Report 19:67-69.

  3. Zhang, X. P., H. T. Skorupska, and B. Rhodes. 1994. Cytological expression in the male-sterile ms mutant in watermelon. Journal of Heredity 85:279-285.

  4. Zhang, X. P., and M. Wang. 1990. A genetic male-sterile (ms) watermelon from China. Cucurbit Genetics Cooperative Report 13:45.

Table 1. Watermelon differentials useful for identification of Fusarium wilt races 0, 1, and 2.

Cultivar Race 0 Race 1 Race 2

'Black Diamond', 'Sugar Baby' S S S

'Quetzali', 'Mickylee' R S S

'Charleston Gray' R M S

'Calhoun Gray' R R S

PI 296341, PI 271769 R R R

S=susceptible, M=moderately resistant, R=resistant. Fusarium wilt is caused by Fusarium oxysporum Schlechtend.:Fr. f. sp. niveum (E.F. Sm.) W.C. Snyder & H.N. Hans.

Figure 1. Watermelon seeds covered by an additional layer of fleshy pericarp in Egusi cultivars, as controlled by the eg gene.

Figure 2. Watermelon seed size: 1 = tomato size (watermelon seeds the size of tomato seeds), LL ss tsts or ll ss tsts; 2 = short (or small, 5 mm long), LL ss or ll ss; 3 = medium (7 mm long), LL SS; and 4 = long (or large) (10 mm long), ll SS.

Cucurbit Genetics Cooperative Report 28-29: 52-61 (2005-2006)

Каталог: cgc -> cgc2829
cgc2829 -> Systematic Studies on the Family Cucurbitaceae of Eastern Bihar, India M. Ajmal Ali and Arun K. Pandey
cgc -> Germination of Watermelon Seeds at Low Temperature
cgc -> Palacký University, Faculty of Science, Department of Botany, Šlechtitelù 11, 783 71 Olomouc, Czech Republic
cgc -> Gynogenesis in a Dihaploid Line of Cucumber
cgc -> V. Ondřej, B. Navrátilová and A. Lebeda
cgc -> Multiple Shoot Induction from the Shoot Tip Explants of Cucumber
cgc -> Gene List for Cucurbita species, 2004
cgc -> Gene List for Cucurbita species, 2009
cgc -> Variation Among Tropical Pumpkin ( Cucurbita moschata ) Cultivars in Susceptibility to Silverleaf
cgc2829 -> Systemic Resistance against Sphaerotheca fuliginea in Cucumber by Cell Fungal Fragments of Flammulina velutipes

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