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Cucurbit Genetics Cooperative Report 6:29-31 (article 15) 1983

Screening Cucumber for Resistance to Belly Rot Caused by Rhizoctonia solani

J. T. Sloane, T. C. Wehner, and S. F. Jenkins, Jr.

North Carolina State University, Raleigh, NC 27650

Belly rot of cucumber (Cucumis sativus L.) caused by Rhizoctonia solani Kuhn is an important disease in the southern U.S.A. The average annual loss of cucumbers to belly rot in the U.S. was estimated to be 7 to 9% (5). A limited degree of control can be obtained by the use of mulches and/or fungicides (2, 3), as well as plowing to a 0.20 to 0.25 m depth before planting (2). Regardless of the control methods used however, Rhizoctonia solani Kuhn, being a soil inhabitant, becomes quickly re-established (1, 4).

Host resistance would be an economical method of control if a source of resistance were found. Single gene resistance has not been identified, but low to moderate levels of resistance exist in some lines. Therefore, recurrent selection appears to be the best approach. The objectives of this study were to develop methods for screening for belly rot resistance, and to identify sources of resistance to be used in a recurrent selection program.

Methods. The four isolates of Rhizoctonia solani Kuhn used in these studies were collected by Dr. S. F. Jenkins. The isolates were tested for pathogenicity, and then increased on potato dextrose agar. Inoculum was produced by introducing pieces of the inoculated agar 1 cm2 into heat-resistant bags containing 300 ml of oat grains and 200 ml of water, all of which had been previously autoclaved. That inoculum, at the rate of 1600 grains/m2 (1 grain/in.2) of surface soil, was used for the 1981 study. All other studies used a rate of 3200 grains/m2. All tests were run on fruit having a diameter of approximately 55 mm, usually considered to be oversize for both pickling and slicing types. All fruit were scored 6 to 12 days after inoculation for percent of the fruit infected with lesions (number of lesions was not a useful scoring method).

In the 1981 initial tests, a single 3 m plot of each of 1063 Cucumis lines (mostly cucumbers) was planted at the Horticultural Crops Research Station at Clinton, North Carolina on May 27. One oversize fruit was harvested on July 21 from each plot and taken to Raleigh. Fruit were placed on greenhouse soil beds that had been inoculated with Rhizoctonia solani, and scored 6 days later for percent lesions.

In the 1982 lab test, plastic flats (450 x 520 mm) were filled to a depth of approximately 50 mm with steam sterilized soil. The most resistant and most susceptible lines from the 1981 test, along with several check lines (174 lines in all), were planted June 7, 1982 in 1.5 m plots at the Central Crops Research Station at Clayton, North Carolina. Oversize fruit free of lesions were harvested, taken to the lab and placed in flats so that neither the blossom nor the peduncle end were touching the soil surface. The flats were then watered and covered with newspaper. The soil was kept damp by daily misting. Temperatures in the greenhouse ranged from 24°C at night to 33°C during the day. After 12 days, the fruit were scored individually for percent lesions. The experiment was a completely random design with 174 lines and 3 replications.

The 174 lines in the 1982 greenhouse test were also tested in the field to verify their disease reaction. The lines were planted on May 13, 1982 at the Horticultural Crops Research Station at Clinton, North Carolina in a randomized complete block design with 2 replications. Each line was planted in 1.5 m plots on 1.5 m centers with 1.5 m alleys between plots. Plots were inoculated at ‘tip-over’ and ratings were made on individual fruit selected randomly from the plot 19, 24, 30 and 34 days later.

Results. Data from the 1981 and 1982 laboratory tests and from the 1982 field test were used to select the lines that were consistently resistant or susceptible. Ten resistant lines and 7 susceptible lines were identified for further testing in 1983 (Table 1). Most of the lines selected were plant introductions and may, therefore, be segregating for resistance. Most of the resistant lines were pickling cucumber types with tender skin, so resistance does not appear to be linked with undesirable fruit characteristics. The line PI 163216 had 0% fruit damage in all 3 of the tests and should be investigated further.

Table 1. Belly Rot resistance (percent of fruit surface infected) and fruit characteristics of the 10 most resistant and 7 most susceptible lines from 2 laboratory and 1 field test.

 

 

 

Percent of fruit surface infected in 3 separate tests

Rank

Cultivar or Line

Origin

Lab
1981

Lab
1982

Field
1982

Fruit
typez

Spine
colory

   1

PI 163216

India

0

0

0

S

B

   2

PI 285606

Poland

0

-

0

P

W

   3

PI 271328

India

0

-

0

P

B

   4

PI 357852

Yugoslavia

0

-

0

S

S

   5

PI 280096

USSR

0

-

0

P

B

   6

PI 197088

India

0

-

0

P

B

   7

PI 212985

India

0

-

-

P

B

   8

Mariner

Joseph Harris

0

-

-

P

W

   9

P 51

Hollar

0

-

-

S

W

  10

Pioneer

Northrup-King

0

1

0

P

W

 

 

 

 

 

 

 

 

1057

PI 344433

Iran

25 

-

16 

S

B

1058

PI 267741

Japan

0

1

13 

S

S

1059

PI 181752

Syria

35 

2

18 

S

S

1060

PI 418962

China

0

3

8

-

-

1061

PI 177360

Turkey

0

10 

9

S

B

1062

PI 169382

Turkey

1

12 

8

S

B

1063

PI 419108

China

0

12 

7

S

W

LSD (5%)

7.2

8.9

 

 

Mean (all lines)

3.1

3.3

 

 

CV (%)

11.5

12.6

 

 

z Fruit type: P = pickle, S = slicer.

y Spine color: B = black, W = white, S = segregating.

Correlations were run for belly rot resistance of the lines in the 3 tests. None of the correlations was significant, and most were near zero. That indicates that the 3 tests varied in the way the lines reacted in each. The non-significant correlations among test results may also have been due to missing data, especially for the susceptible lines which were often eliminated from the tests by other diseases such as anthracnose.

Literature Cited

  1. Lewis, J. A., R. L. Dow, W. A. Avers, and J. G. Kantzes. 1979. Ecology and epidemiology of Rhizoctonia solani in field soil. Phytopathology 68:871–877.
  2. Lewis, J. A. and G. C. Papavizas. 1980. Integrated control of Rhizoctonia fruit rot of cucumber. Phytopathology 70:85–89.
  3. Jones, J. P. 1961. Comparative effects of soil fungicide treatments on soil rot and damping off of cucumber. Plant Dis. Reptr. 45:376–379.
  4. Parmeter, J. E. (Ed.). 1970. Rhizoctonia solani: biology and pathology. University of California Press, Berkeley.
  5. Sumner, D. R. and D. A. Smittle. 1976. Etiology and control of fruit rot of cucumber in single harvesting for pickles. Plant Dis. Reptr. 60:304–307.
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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 1 August, 2007