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Cucurbit Genetics Cooperative Report 14:92-97 (article 33) 1991

R309, A Selection of Citrullus colocynthis with Mutagenic Resistance to Colletyotrichum lagenarium race 2

S.L. Love and B.B. Rhodes

Assistant Professor, University of Idaho, Aberdeen ID 83210 and Professor, Clemson University, Clemson, SC 29632, respectively

Anthracnose, caused by Colletotricum lagenarium (Pass.) Ell. and Halst., is a widespread disease of cucurbits (5). It is especially destructive on watermelon (Citrullus lanatus (Thunb.) Matsum and Nakai) in humid growing regions of the world. The discovery of anthracnose reistance has been reported (5, 7, 8, 9). On 1980, Sowell et all. (7) screened 450 plant introductions of C. colocynthis for resistance to race 2 C. lagenarium. Suvanprakorn et al. (8) concluded that three of these, PI 271778, PI 326515 and PI 189225, had a single dominant gene for resistance.

Seven races of C. lagenarium have been described (2, 3, 4). Resistance to races 1, 3 and 7 have been incorporated into commercial watermelon cultivars. The predominant race of C. lagenarium in the Southeastern United States is now race 2. A shift in race prevalence from race 1 has made the use of expensive fungicides the only effective control measure (4).

The use of single gene resistance to eliminate the threat of anthracnose invites the same sequence of events, namely a rapid change in race prevalence, as occurred previously (1). This paper introduces the selection R309, a new source of resistance to race 2 C. lagenarium with multigenic resistance.

R309, the resistant line characterized in this study, is a selection of C. colocynthis. Citrullus colocunthis crosses easily with C. lanatus and only occasionally results in sterility or genetic abnormality. Two additional genotypes, the resistant PI 189225 and the susceptible cultiva New Hampshire Midget were included as parents. PI 189225 was included to provide direct comparison with previous work (8, 9). The study was conducted in the field in 1983. Seed from, each parent, recioprocal F1, F2 and BC generations, were planted in a randomized complete block with four replications.

An isolate of C. lagenarium was obtained from naturally infected watermelons at the Edisto Research and Education Center in Blackville, SC. Using hot differentials (4), the isolate was determined to be race 2. Methods used for culture of the fungus and spore production were adapted from Littrell and Epps (6). The plots were inoculated at sundown by spraying six-week old plants with a suspension of 20,000 conidia-1. After five weeks, the mature vines were rated for resistance using a two-part rating system. The rating system combined the percent defoliation with the precent of remaining leaves showing lesions. This resulted in a zero to 200 scale (0 = immune, 200 = dead). Plants with a score of 70 or less were considered resistant; polants with scores greater than 70 were considered susceptible.

Chi-square analysis was used to determine if resistance ws simply inherited. Orthogonal contrasts were also used to clarify the relationships among parents and F1 populations.

In the inheritance study R309 demonstrated the same level of resistance for which it had been selected at the Edisto Research and Education Center. A mean rating score of 48.7 was recorded, which was slightly higher (more susceptible), than the score of 25.5 for PI 189225 and much lower than the 115.2 recorded for New Hampshire Midget. This level of resistance is more than adequate for commercial production of waermelons without the use of fungicides.

Chi-square analysis of progeny from PI 189225 x New Hampshire Midget confirmed the conclusion of Suvanprakorn et al. (8) that resistance from this source is due to a single dominant gene.

Chi-square analysis revealed a poor fit for a single dominant gene hypothesis in the progeny of R309 (Table 1). Neither did the data fit a two dominant gene model. From the observed ratios, it was concluded that the resistance of R309 is multigenic in nature. This type of resistance has not been available for breeding resistance to race 2 C. lagenarium and may prove valuable.

The actual inheritanceof the resistance expressed by R309 has not been determined but orthogonal contrasts were used to provide more information (Table 2). Reciprocal 1 (R 309 x NHM) populations were not significantly different indicating that resistance is due to nuclear rather than cytoplasmic genes. The parent R309 and the F1 (R 309 x NHM) were not significantly different, but the F1 was significantlymore resistant than the midparent, indicating that resistance in R309 is due to complete dominance.

Due to the small difference in resistance between PI 189225 and R309, Chi-square analysis could not define the genetic relationship of the resistance found in each line. Comparison of progeny means from R309 x PI 189225 indicated that the level of resistance displayed by PI 189225 is higher and is also due to dominance (Table 3). The gene(s) that impart a higher level of resistance to PI 189225 is presumably the same dominant factors described previously (8).

In conclusion, R309 is a selection of C. colocynthis with intermediate resistance to race 2 C. lagenarium. The genes conditioning resistance in R309 are different from any previously reported. Multiple dominant genes are responsible for the resistance expressed by R309 and the use of an appropriate breeding scheme should make it possible to successfully exploit this new source. It is likely that this multigenic source of resistance will be more stable than single gene sources.

Table 1. Reaction of R309, 'New Hampshire Midget' (NHM) watermelon and progeny to inoculation with C. lagenarium race 2 in the field. Chi-square test for single gene resistance.

Total Plants
Expected Ratio
20 - .50
BC x R309

aAll plants were rated on a 0 to 200 scale (0 = no symptoms; 200 = dead). Plants with a score of 0 to70 were considered resistant; those above 70 susceptible.

Table 2. Disease rating of R309, New Hampshire Midget (NHM), F1 and midparent in the 1983 field study.

NHM vs R309
R309 vs F1
F1 vs midparent

aPlants were rated on a) to 200 scale (0 = no symptoms; 200 = dead). Plot means are given.
bNonsignificant (ns) or siognificant at the 5% (*) or 1% (*) level. Comparisons were made using orthogonal contrasts.

Table 3. Disease rating of R309, PI 189225, F1 and midparent in the 1983 field study.

PI 189225
R309 vs PI 189225
PI 189225 vs F1

aPlants were rated on a 0 to 200 scale (0 = no symptoms, 200 = dead).
bNonsignificant (ns) or significant at the 5% (*) or 1% (**) level. Comparisons were made using orthogonal contrasts. 

Literature Cited

  1. Crall, J.M.. History and present status of watermelon improvement by breeding. Proc. Soil Sci. Soc. Florida 13:71-74.
  2. Dutta, S.K., C.V. Hall and E.G. Heyne. 1960. Observations on the physiological races of Colletrotrichum lagenarium. Bot. Gaz. 121:163-170.
  3. Goode, M.J. 1958. Physiological specialization in Colletotrichum lagenarium. Phytopathology 48:79-83.
  4. Jenkins, S.F., Jr., N.N. Winstead and C.L. McCombs. 1964. Pathogenic comparisons of three new and four previously described races of Glomerella cinqulata var. orbiculare. Plant Dis. Rep. 48:619-622.
  5. Layton, D.V. 1937. The parasitism of Colletotrichum lagenarium (Pass.) Ell and Halst. Iowa Agr. Exp. Stat. Bull. 223.
  6. Littrell, R.H. and W. M. Epps. 1965. Standardization of a procedure for artificial inoculation of cucumbers with Colletotrichum lagenarium. Plant Dis. Rep. 49:649-653.
  7. Sowell, G., Jr. B. B. Rhodes and J.D. Norton. 1980. New sources of resistance to watermelon anthracnose. J. Amer. Soc. Hort. Sci. 105:197-199.
  8. Suvanprakorn, K. and J.D. Norton. 1980. Inheritance of resistance to race 2 anthracnose in watermelon. J. Amer. Soc. Hort. Sci. 105-862-865.
  9. Winstead, N.N., M.J. Goode and W.S. Barham. 1959. Resistance in watermelon to Colletorichum lagenarium races 1, 2, and 3. Plant Dis. Rep. 43:570-576.
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Page citation: Wehner, T.C., Cucurbit Genetics Cooperative;
Created by T.C. Wehner and T. Ng, 1 June 2005; design by C.T. Glenn;
send questions to T.C. Wehner; last revised on 14 December, 2009