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Cucurbit Genetics Cooperative Report 15:19-21 (article 8) 1992

Screening Cucumber for Resistance to Belly Rot Caused by Rhizoctonia solani

Todd C. Wehner, Michael S. Uchneat and Rufus R. Horton, Jr.

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

Belly rot caused by Rhizoctonia solani Kuhn (Ag-4) is one of the more important cucumber (Cucumis sativus L.) diseases in the southeastern United States. Crop loss in the southern United States averaged 7 to 9%, with potential yield loss of up to 80% (3). In North Carolina, the average annual loss was approximately 3.5% (4).

Efforts to control belly rot, which have been primarily by chemical means in the past, were generally unsuccessful or inefficient (2, 3). Resistant cultivars would provide adequate and economical protection. Therefore, in these experiments we were studying resistance available in the gene pool. In a series of experiments over several years, the majority of the cucumber germplasm collection has been screened using field and detached fruit tests (5, 7). That has provided a good base of information for future breeding work.

The narrow-sense heritability for resistance to belly rot was estimated at 0.24, which is low to moderate heritability (6). Thus, resistance could be transferred to horticultural acceptable material, provided that resistant germplasm can be identified.

Damping off, which can also be caused by R. solani, has also been studied as a method of screening for resistance to belly rot. Booy et al. (1) found that resistance to damping off was not correlated with either field or detached fruit tests. This indicates that this method could not be used to screen for belly rot resistance.

The objective of this study was to screen the cucumber germplasm collection to detect large differences in resistance, and to identify the best sources of resistance to belly rot to use in further studies.

Methods: Two methods were used to screen for belly rot resistance, field and detached-fruit tests. Field tests were conducted at the Horticultural Crops Research Station, Clinton, NC. Detached-fruit tests were conducted in a greenhouse in Raleigh, NC. Tests were run in 1981 through 1985. Work done in 1984 dealt with inoculum concentration and further improvement of the test method, and will not be presented here. Experiment design, inoculum concentration, and dates of planting and harvest are given in Table 1.

The field tests involved replicated plots of the cultigens of interest, with R. solani infested oat grains added to the soil surface at the vine-tip-over stage (6 to 9 nodes). When fruits were of the appropriate size (50 mm diameter) they were rated for percentage infected with R. solani.

Inoculum was prepared by first autoclaving 300 cm3 of oats and 250 ml of water for 1 hour for two consecutive days in autoclavable bags. R. solani colonized potato dextrose agar disks approximately 1 cm2 were transferred to the sterile oats and allowed to incubate for 7 days. Once colonized, the oats were dried and stored at 4°C until needed (7).

Detached-fruit tests consisted of growing plants in the field and harvesting fruits for testing in a closed chamber. Flats were filled with steam-sterilized field soil and infested with R. solani by adding colonized oat grains. Fruits were then dipped in 10% Clorox (0.52% NaOCl), placed on the flats kept in a growth chamber maintained at greenhouse temperature and high humidity. We did not follow the Clorox dip with a water rinse (to avoid spreading disease). Temperatures averaged 35°C day and 27°C night, Humidity was not controlled except through the use of a closed chamber.

The soil was moistened at the start of the experiments and allowed to dry out for 3 days before re-wetting. Soil moisture was not critical for good disease development as long as the soil did not become completely dry (unpublished data). Fruits were rated as close to 7 days after inoculation as possible, although it was sometimes necessary to use shorter (4 days or longer (12 days) periods to allow for proper development of disease symptoms.

Fruit were rated by estimating the percentage of the fruit surface that was colonized by the fungus. A rating of 30% indicated that the entire belly of the fruit was colonized. Ratings greater than 30% occurred when the fungus spread throughout the fruit. Primary symptoms consisted of brown, sunken, necrotic lesions. Rhizoctonia or secondary pathogens often colonized susceptible fruit so they acquired a soft and mushy appearance. Data were standardized to the same environments. However, since the most resistant and susceptible cultigens were not included in all tests, the original data provided a better estimate of resistance. Therefore, we used unstandardized data for analysis and presentation.

Results: Cultigens with no fruit damage in any of the years tested were PI 197088, PI 357852, PI 280096, and 'P 51' (Table 2). Cultigens showing the greatest susceptibility were 'Supergreen', PI 419108, PIO 163218 and {O 177360 (Table 2). Most cultigens were not tested in all years, so care must be used in interpreting relative resistance. Fruit damage was variable as indicated by the highly coefficients of variation (CV) in all of the experiments. We believe environmental conditions played a large role in that variability.

The check cultivar Marketmore 76 was shown to have good resistance. Slicing cucumbers like 'Marketmore 76' have tough skin for shipping. There appears to be a relationship between skin toughness and belly rot resistance. Also, PI 197088 had good resistance and a brown, netted skin. PI 163216 and PI 177360 differed in resistance in field and detached tests (Table 2). The correlation between field and detached-fruit tests was not significant in 1982 (r = 0.07), and significant in 1983 (r = 0.50).

Other potential problems with these experiments is the fact that all fruit do not mature at the same time. This leads to problems at the time of rating when fruits are not all of equivalent size and age. Later-maturing cultigens will often be rated for resistance using small, immature fruits. To correct for that problem, it would be useful to have a technique for screening at the seedling stage.

This study demonstrates the large differences in belly rot resistance in the cucumber germplasm collection. From this data it is possible to select resistant parents and susceptible checks for further study. Future work needs to be done to verify the sources of resistance and to improve the test methods.

Table 1. Experiment design and methods used in evaluating cucumber cultigens for resistance to belly rot (1981-1985).

Year
Test typez
No. cult
No. reps
No. fruity
Inoc. conc.x
Date
1981
Det
1063
1
1
1600
27 May
25. 28 July, 1 Aug.
1982
Fld
174
2
3
3200
13 June
1, 6, 12 Aug.
 
Det
174
3
3
3200
7 June
13, 16, 18, 21 June
1983
Fld
149
2
2
4800
24 May
11, 18, 25 July, 4 Aug.
 
Det
149
3
3
4800
13 May
15, 25 July
1985
Fld
85
3
8
4800
29 April
5, 11 July
 
Det
85
3
4
4800
29 April
24 July

z Det = detached fruit; Fld = Field test.
y Number of fruits per replication.
x Inoculum concentration in grains per m2.
w Fruits for detached test were harvested 4 to 12 days before rating.

Table 2. Belly rot resistance of resistant, susceptible and check cultigens tested 1981 through 1985.z

     
Field test
Detached test
Cultigen
Seed source
Meany
1982
1983
1985
1981
1982
1983
1985
Resistant  
PI 197088 India
0
0
0
-
0
0
0
-
PI 357852 Yugoslavia
0
0
0
-
0
0
-
-
PI 280096 USSR
0
0
-
-
0
0
-
-
PI 285606 Poland
0
0
-
-
-
0
-
-
PI 271328 India
1
0
2
-
0
1
1
-
PI 279282 Yugoslavia
1
0
-
-
0
3
-
-
PI 163216 India
1
0
2
2
0
0
0
5
Check cultigens
P51 Ferry-Morse
0
0
-
-
0
-
-
-
Marketmore76 Cornell Univ.
1
-
-
1
-
-
-
1
Pioneer Clemson Univ.
1
0
2
-
0
1
1
-
Guardian Rogers NK
2
-
-
1
-
-
-
2
M 21 NC State Univ.
2
-
-
2
-
-
-
1
M 16 NC State Univ .
2
-
-
1
-
-
-
3
Castlemaster SunSeeds
2
-
-
2
-
-
-
2
Poinsett 76 Cornell Univ.
2
-
-
2
-
-
-
2
Wautoma Wis-USDA.
2
-
-
2
-
-
-
2
Calypso NC State Univ.
3
-
-
2
-
-
-
4
Little John Univ. Ark.
4
-
-
2
-
-
-
5
Sumter Clemson Univ.
4
-
-
3
-
-
-
4
Score Asgrow Seed
4
-
-
4
-
-
-
3
Carolina Clemson Univ.
4
-
-
3
-
-
-
5
Wis. SMR 18 Univ. Wis.
5
-
-
4
-
-
-
5
WI 1701 Wis-USDA
5
-
-
4
-
-
-
6
WI 2757 Wis-USDA
15
-
-
6
-
-
-
23
Supergreen Harris-Morgan
22
-
-
10
-
-
-
34
Susceptible
PI 344433 Iran
5
5
-
-
-
-
5
-
PI 418962 China
5
6
-
-
3
9
0
-
PI 267741 Japan
5
8
-
-
2
-
5
-
PI 177360 Turkey
6
1
-
-
5
9
10
-
PI 169382 Turkey
10
12
-
-
8
12
6
-
PI 181752 Syria
12
10
-
-
23
4
-
-
PI 419108 China
14
-
-
11
8
15
6
30
Mean  
3
4
3
-
3
3
7
LSD (5%)  
9
7
3
-
7
7
11
CV (%)  
115
76
54
-
126
84
77

z Data are mean percentage of fruit surface damaged by belly rot.
y Mean across experiments without standardizing data.

Literature Cited

  1. Booy, G., T.C. Wehner and S.F. Jenkins, Jr. 1987. Resistance of cucumber lines to Rhizoctonia solani damping off; not related to fruit rot resistance. HortScience 22: 105-108.
  2. Halterlein, A.J., G.L. Sciumbato and W.L. Barrentine. 1981. Use of plant desiccants to control cucumber fruit rot. HortScience 16: 189-190.
  3. Lewis, J.A. and G.C. Papavizas. 1980. Integrated control of Rhizoctonia fruit rot of cucumber. Phytopathology 70: 85-89.
  4. Main, C.E. and S.M. Nusser. 1985. 1984 estimates of crop losses in North Carolina due to plant diseases and nematodes. North Carolina State University, Raleigh, Dept. of Plant Pathology Special Pub.
  5. Sloane, J.T., T.C. Wehner and S.F. Jenkins, Jr. 1984. Evaluation of screening methods and sources of resistance for Rhizoctonia fruit rot in cucumber. Cucurbit Genet. Coop. Rpt. 7: 23-24.
  6. Sloane, J.T., T.C. Wehner. 1985. Inheritance of resistance to Rhizoctonia fruit rot in cucumber, Hort Science 20: 1119-1120.
  7. Wehner, T.C. and S.F. Jenkins. 1986. Field and detached-fruit tests for resistance of cucumber lines to fruit rot caused by Rhizoctonia solani. Cucurbit Genet Coop. Rpt. 9: 41-43.
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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 15 December, 2009