Triploid Watermelons Resist Fruit Blotch Organism

Cucurbit Genetics Cooperative Report 18:56-58 (article 27) 1995

J.T. Garret, B.B. Rhodes and Xingping Zhang
Department of Horticulture, Clemson University, Clemson, SC 29634

Watermelon fruit blotch disease (WFB), presently attributed to the bacterium Acidovorax avenae subsp. citrulli, is a devastating disease which renders infected watermelon [Citrullus lanatus (Thunb.) Matsumura and Nakai] fruits unmarketable. This disease is transmitted initially through infected seed (3) and secondarily by mechanical means of water movement and direct contac emanating from cultural operations (5). Favorable environmental conditions of high relative humidity, warm temperature and frequent rainfall may cause WFB to rapidly reach epidemic proportions. Symptoms may appear within 72 h after the inoculum contacts immature fruits (5). The potential for spread is exacerbated by establishing the crop with greenhouse grown transplants which were exposed to infected seedlings.

Somodi et al. (5) described the symptoms on watermelon fruit as large, firm, dark-green, water-soaked lesions with irregular margins, symptoms also occurred on foliage. These workers found the bacterium to be similar but not identical to Pseudomonas pseudocalcaligenes subsp. citrulli, a previously described pathogen on watermelon. Lesions developed on all 36 cultivars in their test. In another study with 22 cultivars, Hopkins et al. (2), reported a gradation of resistance with light colored rind types being more susceptible than dark green rind types. Rhodes et al. (4) used WFB to inoculate the three genotypes reported most resistant to P. pseudoacalcaligenes subsp. citrulli by Sowell and Schaad (6), and found resistance in PI 295843 and foundation seed of ‘Congo’.

In previous outbreaks of WFB, we observed no damage to triploids in the vicinity of infested plantings. We were uncertain if this difference was due to resistance or absence of the organism.

In this experiment, our initial objective was to compare several commercially available triploid watermelon cultivars with tissue cultured lines for plant vigor, yield and fruit quality. Coincidentally, WFB symptoms appeared and different responses between diploid and triploid cultivars are reported here.

Materials and Methods:A field study was established 17 May 1994 at the Pee Dee Research and Education Center, Florence, SC,on a Norfolk loamy sand soil (a structureless, fine, loamy, siliceous, thermic, Typic Kandiudult) with pH 6.0). Twenty triploid cultivars, using greenhouse grown transplants, were evaluated in a replicated trial. Diploid watermelons (‘Crimson Sweet’ and ‘SC-7’) were utilized as pollinizers.

The experimental design was a randomized complete block of four replications. Plots were 15.24 m long and within-row plant spacing was 1.5 m. Rows were spaced 1.83 m apart. The plots were prepared for planting in a conventional manner to form 15-cm high, broad, flat-topped beds. Recommended cultural practices for South Carolina were followed (1). Each triploid plot was flanked on either side by a pollinizer row.

Overhead sprinkler irrigation was applied as needed to prevent moisture stress. As the test approached maturity, cloudy days with frequent precipitation predominated (12 days with measurable precipitation during the 21 days prior to harvest). Harvest was made 8 August 1994, 83 days after transplanting.

Since all pollinizer plants were uniformly infested with WFB, each row of diploid plants was evaluated by randomizing a point on the row from 1 to 50 and rating the diploid fruit nearest that point. The severity rating scale consisted of 1=no blotch; 3=mild blotch, affected area totaling 6.45 cm2 ; 5=severe blotch 6.45 cm2 but no open wounds; 7=open wounds, cracked rind, or decay. Each triploid fruit 3.63 kg and larger was evaluated for WFB symptoms.

Results and Discussion: The field was heavily and uniformly infested with WFB as shown by the percentage of fruits infected in the pollinizer plots (Table 1). Hardly a fruit could be found among the diploids that was not symptomatic of WFB. The severity ranged from mild to open wounds with data being skewed strongly toward the later rating (average 5.42).

All triploid cultivars had fewer fruits affected by WFB (Table 1) with many fruits of some cultivars showing no symptoms. It was not uncommon to have a triploid fruit with no symptoms lying in contact with a diploid fruit with open wounds and rot. The severity of WFB symptoms on triploid fruits was substantially less when compared with diploid fruit symptoms. Rarely was a triploid fruit rated with severe symptoms, and no triploid fruit was found to have open wounds or rot (average rating 3.07). WFB infection for the triploid cultivars ranged from 9.7 to 29.8 percent while the diploids were above 92 percent. The mean infection for all triploids was 18.7 percent.

We conclude from these data that triploid watermelons are more resistant to the WFB organism than diploid watermelons. The difference among triploids is sufficient to be exploited.

Table 1. Responses of triploid and diploid watermelons to watermelon fruit blotch organism.

Genotypes

Percentage of infection (%)

Severity of symptomsz

Diploids

SC – 7 95.0 ay 5.75 a
Crimson Sweet 92.3 a 5.09 ab

Triploids

Nova 29.8 b 3.55 bc
Triten 24.9 b 3.28 bc
Jack of Hearts 23.4 b 3.46 bc
King of Hearts 22.9 b 3.40 bc
Tri-5 22.3 b 3.27 bc
93-CUT-1 21.6 b 3.06 bc
Queen of Hearts 21.4 b 3.34 bc
Deuce of Hearts 21.2 b 3.47 bc
AC-5244 20.5 b 3.43 bc
Honeyheart 19.6 b 3.18 bc
ACR-94W003 18.9 b 3.30 bc
Tri-3 17.0 b 3.25 bc
93-Delta-3 16.7 b 2.50 c
Crimson Jewel 15.8 b 3.35 bc
Ace of Hearts 15.7 b 2.49 c
ACR-92W036 15.0 b 3.25 bc
AC-2532 13.7 b 1.81 c
93-CUT-2 13.2 b 3.00 bc
AC-3731 10.6 b 2.67 c
ACR-94W001 9.7 b 2.25 c

zRating scheme. 1=no blotch, 3=mild blotch, affected area totaling 6.45 cm2; 5=severe blotch 6.34 cm2 but no open wounds’ 7=open wounds, cracked rind, or decay.
y Mean separation within columns by Duncan’s Multiple Range Test; P=0.01.

Literature Cited

  1. Cook, W.C., C.E. Drye and R.P. Griffin. 1980. Growing Watermelons in South Carolina. SC Ext. Set. Bul. 121.
  2. Hopkins, D.L., C.M. Thompson and G.W. Elmstrom. 1993. Resistance of watermelon seedlings and fruit to the fruit blotch bacterium. HortScience 28:1-2.
  3. Rane, K.K. and R.X. Latin. 1992. Bacterial fruit blotch of watermelon: Association of the pathogen with seed. Plant Dis. 76:509-512.
  4. Rhodes, B.B., N.V. Desamero and Xingping Zhang. 1991. A strategy toward varietal resistance to watermelon fruit blkotch, Cucurbit Genet. Coop. Report 14:102-103.
  5. Somodi, G.C., J.B. Jones, D.L. Hopkins, R.E. Stall, T.A. Kucharek, N.C. Hodge and J.C. Watterson. 1991. Occurrence of a bacterial watermelon fruit blotch in Florida. Plant Dis. 75:1053-1056.
  6. Sowell, Grover, Jr., and N.W. Schaad. 1979. Pseudomonas pseudoalcaligenes subsp. citrulli on watermelon: Seed transmission and resistance of plant introductions. Plant Dis. Rept. 63:437-441.