Ann. appl. Biol. (1985). 106, 413-422 Printed in Great Britain

413

Stem canker (Rhizoctonia solani) of maincrop potatoes. I. Development of the disease

BY G. A. HIDE, P. J. READ AND JANET P. SANDISON Rothamsted Experimental Station, Harpenden, Herts., AL.5 2JQ

(Accepted 18 December 1984)

SUMMARY

In two years, potato plants were sampled at 1- or 2- weekly intervals from plots planted with seed tubers bearing sclerotia of Rhizoctonia solani (black scurf) and with seed without sclerotia either infested or not with cultures of R. solani at planting. Sprouted King Edward seed was used in 1981 and sprouted and non- sprouted King Edward and Pentiand Crown seed in 1982.

In both years 60-80% of shoots from seed with sclerotia and 90% of shoots from seed inoculated at planting were affected with stem canker. Most disease developed before shoots emerged although it gradually increased later when new shoots arising both from seed tubers or as branches on shoots with damaged apices (pruned shoots) became infected before they emerged. Sprouting seed tubers bearing sclerotia decreased the disease on both cultivars but with soil-applied inoculum the disease was more severe on plants from sprouted than non-sprouted seed.

Some stolons were infected by R. solani soon after they developed and incidence of infection later increased. Thirty to 50% of stolons were infected on plants from infected seed tubers and 60% on plants with soil-applied inoculum. With both cultivars and sources of inoculum about 70% of the infected stolons had their apices killed (pruned).

INTRODUCTION

Infection of potato plants by Rhizoctonia solani Kiihn, mycelial state of Thanatephorus cucumeris (Frank) Donk, is found wherever the crop is grown. In some areas, where potatoes are produced in monoculture or in short rotations, soil populations of the fungus can be an important cause of infection (Sadowski & Zawislak, 1975; Frank, 1978). In most areas, however, stem canker originates from sclerotia (black scurf) on seed tubers (Harrison, 1978) and, as treating seed tubers with fungicides prevents mycelial growth from sclerotia, the disease can be readily controlled (Hide & Cayley, 1982).

The experiments reported here and in a following paper (Hide, Read & Sandison, 1985) were made to investigate development of stem canker disease on two maincrop potato cultivars and how it affects growth of foliage and tubers, using plants from infected seed tubers and, to ensure severe infection, plants from seed tubers grown in soil inoculated with R. solani at planting.

MATERIALS AND METHODS

Production of seed tubers Sprouted seed tubers (FSI certificate) were planted by hand at Rothamsted in 1980 (King

Edward) and 1981 (King Edward, Pentland Crown) and before covering, cultures of R. solani, isolated from a stem canker lesion in 1976, maintained on 2% malt extract agar at 5°C and 0 1985 Association of Applied Biologists

414 G . .4. H I D E , P . J . R E A D A 3 D J A N E T P . S A N D I S O N

grown for 6 wk at 15°C on horticultural vermiculite moistened with 2% malt extract solution, were sprinkled over tubers in furrows at 140 ml m-I row. Samples of seed without inoculum were planted in an adjacent plot. Granular insecticide (phorate) was applied at planting and crops were sprayed regularly with insecticide (demeton-S-methyl) and with fungicide (mancozeb) to protect against late blight. After lifting in October tubers from inoculated and non-inoculated plots were stored separately at 5°C.

Experiments in 1981 and 1982

All seed tubers were washed in January (1981) or February (1982). Tubers with black scurf (1981, King Edward 3-5% surface affected; 1982, King Edward 4%, Pentland Crown 3%) were selected from crops grown with inoculum, and those without black scurf from non- inoculated plots. In 1981, all tubers were graded into sizes (mean tuber weights 32, 48, 66, 87. 1 1 1 , 195 g), stored on trays at 7°C in fluorescent light to sprout and planted on 22 Apiil. Seed tubers were graded into two sizes (78, 108 g) in 1982 and half the number of each size was sprouted on trays and half held at 2°C in the dark (non-sprouted) until planting on 20 April

I n 1981 the experiment comprised six randomised blocks (seed tuber size) of three inoculum treatments on King Edward; (1) seed tubers without black scurf (no inoculum), (2) seed tubers with black scurf (seed-borne inoculum) and (3) seed tubers without black scurf but inoculated at planting with cultures of R . solani as previously described (soil-applied inoculum). These inoculum treatments were used in 1982 with seed tubers of King Edward and Pentland Crown either sprouted or not sprouted and planted in two randomised blocks (seed tuber size). In both years plots were four rows (91 cm wide) of 50 plants spaced at 38 cm and in 1982 guard rows were planted with sprouted or non-sprouted seed tubers as appropriate.

Sampling In both years eight-plant samples (two plants from four adjacent rows) were dug on 16

dates, usually at 1- or 2- wk intervals, from randomised positions in each plot. Stem canker was recorded on all stems by grading each lesion on the extent of the stem circumference affected viz. 1 , lesion up to 2 mm wide; 2, from 2 mm to 25% of stem affected; 3, from 25 to 50R; 4. from 50% to almost girdled; 5, lesion extending round whole circumference. The length of each lesion was measured. Products of length and severity grade were summed and, from the total length of all stems below soil level, a disease score for each plot was calculated as a percentage of the maximum possible (all stems with lesions of grade 5 over their whole length). Shoots completely girdled and severed by lesions (pruned) were recorded separately and were not included in the disease score.

Stolons were counted and the numbers with lesions or completely girdled and severed (pruned) recorded. In 1981 the position of nodes on stem bases and the length of stolon were also recorded on samples taken soon after planting.

I n both years, the incidence of black scurf on progeny tubers was recorded on the final sample.

Shoot emergt’nce and stem canker 1981. Samples were first taken 4 wk after planting when shoots had emerged from about

40% of seed tubers of all treatments and stem canker affected about half the number of stems on plants with seed or soil inoculum (Fig. l a ) . More shoots were affected 2 wk later when 95% of plants had emerged, and disease incidence was greatest on plants with soil inoculum. Stem canker score (Fig. l a ) gradually increased between wk 4-12 with most of the increase

100

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Development of stem canker on maincrop potatoes

( a ) 1981, King Edward

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-

Stems affected (7%)

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30

20

10

0 -

w -

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#

40

30

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10

0-

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Disease score (%)

J

(b ) 1982, disease score (%)

Pentland Crown King Edward

’ .- -.--.

415

1 1 I I I I t I L I I I I I I I

2 4 6 8 10 12 14 16 2 4 6 8 10 12 14 16

Weeks after planting Fig. 1. Development of stem canker, 1981 and 1982. 0, no inoculum; 0, seed-borne inoculum; A, soil- applied inoculum; ~ , sprouted seed tubers; - - -, non-sprouted seed tubers.

on plants with soil inoculum occurring during wk 4-6. Eight wk after planting more shoots were pruned with soil (16%) than with seed inoculum (2%). Very few stems on plants without inoculum were affected with stem canker.

1982. Emergence of individual shoots was recorded. Six wk after planting, sprouting the seed tubers had increased the percentage of emerged shoots from both cultivars (Table la ) and, whether seed was sprouted or not, more than 90% of shoots had emerged from seed without inoculum at 7 wk. Numbers of shoots arising from seed tubers were decreased by sprouting especially on King Edward plants (Table lb) and numbers changed little during sampling between wk 6-10.

Six wk after planting seed inoculum had delayed emergence of King Edward shoots from sprouted and non-sprouted seed more than had soil inoculum and, at wk 7, had prevented emergence of 40% of shoots from non-sprouted seed (Table la ) . One third of the shoots from

416 G . A . H I D E . P. J . R E A D A N D J A N E T P . S A N D I S O N

non-sprouted seed with black scurf were pruned off by R. solani at 6 wk (Table l c ) and, although the number of shoots arising from seed tubers increased during wk 8 (Table 1 b) , emergence did not improve, probably because about 30% of these new shoots were subsequently infected and pruned off. Percent shoot emergence from sprouted King Edward seed with soil inoculum decreased after wk 7 when the number of shoots increased (Table 1 b) and one third of shoots were pruned off at wk 8, 2 wk later than with non-sprouted seed.

Table 1. Eflect of seed-borne (seed) and soil-applied (soil) inoculum of Rhizoctonia solani on emergence, numbers and pruning of shoots, 1982

King Edward Pentland Crown Source of inoculum

U'k after Planting

6

X 10

5

7

5

6 7 8

10

i h I

X 10

Not sprouted seed Nil Seed Soil

0 0 0 18 8 14

100 59 71 93 58 89

100 72 92

3 . 8 3 . 7 4 . 2 4 . 4 4 . 8 4 . 9 4 . 3 4 . 4 4 . 6 5 . 1 7 . 8 4.5 5 . 1 7 . 7 3 . 8

0 5 9 0 35 7 0 30 12 0 30 6 1 27 8

Sprouted seed Not sprouted seed Nil Seed Soil Nil Seed Soil

( a ) Q shoots emerged 2 8 2 0 0 0

65 34 60 39 29 4 91 91 90 96 48 65 97 89 50 98 59 50

100 96 62 100 70 48

(6) Number of shoots/seed tuber 1 . 6 3 . 8 3 . 6 5 . 5 6 . 4 4 . 7 3 . 2 3 . 7 3 . 4 4 . 8 5 . 3 4 . 9 4 . 2 3 . 4 3 . 1 4 . 8 6 . 8 4 . 4 4 .4 3 . 9 S . 7 4 .5 6 . 3 6 . 5 3 . 9 3 . 4 5 . 8 4 . 9 6 . 2 6 . 4

(c) 7 shoots pruned by R . solarii 0 3 5 0 5 9 0 3 2 0 4 7 0 7 0 0 34 20 0 6 34 0 29 30 0 3 34 0 30 42

Sprouted seed Nil Seed Soil

8 13 12 75 51 49 95 74 61 94 78 50 98 78 42

3 . 8 4 . 8 1 . 7 4 . 2 5 . 6 4 . 6 4 .1 6 . 5 4 . 5 4 . 4 6 . 1 8 . 0 4 .8 5 .8 7 . 6

0 13 3 0 12 23 0 22 29 0 18 37 0 15 36

S F D

( I 1 D F )

0 . 6 2 0 . 8 5 0 .58 1.01 0 . 9 4

Emergence of Pentland Crown shoots was delayed most by soil inoculum and with both sprouted and non-sprouted seed percentage shoot emergence decreased during wk 7-10 as more shoots were produced from seed tubers (Table l b ) . Simultaneously, with both sources of inoculum shoots were pruned off by R. solani during wk 6-8 but as the number of shoots did not increase on plants with seed inoculum, percent emergence did not decrease.

Three wk after planting about 10% of shoots on plants with seed or soil inoculum were affected with stem canker and by wk 10 about 90% were affected from soil inoculum and 60% (Pentland Crown) or 70% (King Edward) from seed inoculum, an incidence of disease similar to 198 I . On King Edward plants the disease was initially most severe from non-sprouted seed with black scurf (Fig. l b ) but did not increase after wk 6; by wk 8 more had developed on plants with soil inoculum. Source of inoculum did not affect severity of the disease on plants from sprouted seed until wk 8 when it increased on plants with soil inoculum.

Severity of stem canker was not greatly affected by source of inoculum on Pentland Crown plants from non-sprouted seed whereas with sprouted seed the disease developed earliest and was most severe with soil inoculum (Fig. 16).

Sprouting seed tubers with black scurf decreased stem canker on both cultivars whereas with soil inoculum the disease was more severe on plants from sprouted than non-sprouted seed.

Development of stem canker on maincrop potatoes 417

Number and infection of stolons 1981. One third of the total number of stolons produced was present 4 wk after planting

(Fig. 2a) when less than half the plants had emerged shoots; numbers reached a maximum at wk 10 (no inoculum, 37 per plant; seed inoculum, 36: soil inoculum, 32) and were not significantly affected by inoculum treatments on any date. Stolon infection 4 wk after planting was most common with seed inoculum (Fig. 2b), but during the following 2 wk incidence greatly increased especially on plants with soil inoculum which had significantly ( P C O . 01) more infection in all samples taken 6 wk or more after planting. On all dates about 70% of infected stolons were pruned off by R. solani lesions.

King Edward, 1981 King Edward, 1982 Pentland Crown, 1982

( a ) Number of stolons per plant

A

( b ) % stolons infected with R. solani

I I I I I I - Weeks after planting

I I I I I

4 6 8 10 12 14 4 6 8 10 12 4 6 8 10 12

Fig. 2. Numbers of stolons and percentage infected by Rhizortonia solani. A, mean of three inoculum treatments. For other symbols see Fig. 1 .

The mean position of nodes on stem bases and the number and position of stolons on eight- plant samples 4 and 6 wk after planting are shown in Fig. 3; also given are the mean length

41 8 G . .4. H I D E . P . J . R E A D A N D J A N E T P . SANDISON

7 -

18

28

38

38

85

of stolons at each node, excluding those pruned off, and the proportion infected 4, 6 and 8 wk after planting. On all dates more stolons were produced at the lower nodes than near soil level (12 cm from seed tuber); longest stolons were found at lowest nodes at 4 wk and at nodes near soil level 2 wk later. Plants from seed with black scurf had most stolon infection at the base of the stem whereas soil inoculum caused more infection at higher nodes especially in samples taken 8 wk after planting.

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1

12

8 -

3 -

0 -

’?[ 8

- Week 4

14

17 -

33

3

13

20

34

36

1

16 -

13 -

I -

18 -

30 -

. {

4

4

, ‘ I0

Week 6 (0) N o inoculurn

16 :4 ( h ) Seed-borne inoculurn

1 2 =I- I h -+ 28

30 38 $; ( c ) Soil-applied inoculurn

21

22

31

4 2 0 20 6 4 2 0 2 0 4 0 6 0 cm ‘5 ” c ni

Week 8

33

31

85

Stolon length (ern) arid infection with R. solani (%)

1-ig. 3 . Position of nodes on stem bases and number, length and infection of stolons by Khi:octonia solarzi , 4. 6 ,ind 8 wk after planting. King Edward 1981. 0, seed tuber; numbers give the total number of stolons o n eight plants and lengths are means of non-pruned stolons: arrows on “r stolon infection indicate, to the right, ‘7 stolons pruned off and to the left. 9 stolons with lesions but with intact tips.

Development of stem canker on maincrop potatoes 419

1982. Stolons were first found 5 wk after planting; numbers increased during the following 7 wk but were not significantly affected by inoculum and means over inoculum treatments from sprouted and non-sprouted seed are shown in Fig. 2. Sprouting significantly increased numbers of stolons on Pentland Crown plants at 5 wk (P<0-05), 6 and 8 wk (P(O.001) and at 10 wk ( P t 0 . 0 5 ) and, except at wk 5 and 12, there were more stolons than on King Edward plants from sprouted seed.

Some stolons were infected by R. solani soon after they formed and the mean number infected always increased in successive samples. Similarly, the percentage of stolons that were infected on Pentland Crown plants increased throughout sampling and especially on the later-developing plants from non-sprouted seed (Fig. 2c). With King Edward, stolon infection on plants from seed with black scurf did not increase after wk 8 as much as on plants with soil inoculum, indicating that many of the later formed stolons were not infected. With both cultivars and inoculum treatments 70% of the stolons that were infected were also pruned off slightly more were pruned on plants from sprouted (73%) than non-sprouted seed (68%). About 3% of stolons on plants without seed or soil inoculum had lesions caused by R. solani.

Black scurf on progeny tubers In both years soil-applied inoculum caused more tubers to be affected with black scurf than

seed-borne inoculum (Table 2). Sprouting seed tubers with black scurf slightly increased incidence of the disease in 1982 but the mean effect over cultivars was not significant. Although King Edward seed without black scurf was selected as having no inoculum, and few stems on plants from this seed were affected with stem canker, black scurf developed on an appreciable proportion of the progeny tubers.

Table 2. Effect of seed-borne (seed) and soil-applied (soil) inoculum of Rhizoctonia solani on incidence of black scurf (% tubers), 21 wk (1981) or 27 wk (1982) after

planting

lnoculum Nil Seed Soil S E D D F

(a ) 1981

( b ) 1982

King Edward, sprouted seed 1 13 32 6 . 2 10

King Edward, non-sprouted seed 12 14 46 sprouted seed 22 30 49

13.9 11 Pentland Crown, non-sprouted seed 0 20 79

sprouted seed I 44 62

DISCUSSION

Van Emden (1965) suggested that potato shoots become resistant to infection by R. solani when they are under the influence of light but it is not known whether this occurs immediately on emergence or sometime later as the shoots become autotrophic. In these experiments much stem canker developed before shoots emerged but in both years incidence and severity gradually increased later, probably because unemerged shoots became infected. After the apices of shoots were killed, further shoots developed from dormant axillary buds on them and some of these were also infected and had their apices killed; this process was repeated up to five times in 1982 and increased the total length of infected shoot. Death of shoot apices is known to be an important component of the stem canker disease (Hooker, 1978; Gigante, 1969; Bogucka, 1978) and in both years seemed to be the main cause of delay in shoot emergence and production of foliage and tubers (Hide et al., 1985).

420 G . A . H I D E , P . J . R E A D A N D J A N E T P . S A N D I S O N

so 40

30

20

10

0 -

Also, in 1982 new shoots arose from the seed tubers of infected plants 8 wk after planting; some of these became infected and contributed to the stem canker score. Infection delayed shoot emergence but development of these new shoots caused an apparent decrease in emergence when expressed as a percentage of the total number of shoots. Griffith ( 1 984) also found that much stem canker had developed before most plants had produced emerged shoots but later the disease severity index increased. Although he suggested that stems continue to develop symptoms after emergence, it is not clear whether this was due to increase in lesion size, infection of emerged stems hitherto uninfected or, as in our experiments, to infection before emergence of late-developing shoots produced on pruned shoots or from the seed tubers.

Stem canker on plants from sprouted King Edward seed with soil-applied inoculum developed earlier in 1981 than in 1982 although by wk 12 disease severity was similar. More rain fell immediately after planting in 1981 than in 1982 (Fig. 4) and mean soil temperatures at 10 cm depth in the week following planting were respectively 6 . 2 and 9.0"C. Although temperatures rose during the following 7 wk they were always about 2°C lower in 1981 than

- - - -

( a ) 1981 b 20 r

-

'"t 0

- - .- 3 rn

E E

20 r 16-

( b ) 1982

Weeks after planting (p)

Fig. 4. Total weekly rainfall and mean soil temperature at lOcm depth. Rothamsted 1981 and 1982

Development of stem canker on maincrop potatoes 42 1

in the following year. In the heavy clay with flints soil a t Rothamsted, therefore, cool and wet conditions after planting in 1981 might have been expected to be more suitable for stem canker development than warmer and drier conditions in 1982 (Brenchley & Wilcox, 1979).

As found by Glendenning ( 1 9 6 9 , stolon infection increased during plant growth and it also developed earlier in 1981 than in 1982, possibly because of earlier production of inoculum on stem canker lesions. However, more rain fell during the time stolons were being infected in 1982 than in 1981 (wk 4-8) and Glendenning (1965) showed that stolons were initially less susceptible to infection by R. solani under conditions of high moisture. In early samples, inoculum on seed tubers caused more infection of stolons a t the basal nodes on stems and also most delay in emergence than inoculum applied over seed tubers at planting, thus confirming the importance of proximity of inoculum (van Emden, 1965).

Applying inoculum over seed tubers a t planting was not intended to mimic soil-borne inoculum which would be distributed throughout the cultivated soil layer and which seldom causes severe disease if shoots emerge quickly (van Emden, 1965); it was included so that effects on growth and yield could be studied on plants with severe infection (Hide et al., 1985). Because the inoculum was localised round seed tubers, its effects could have been similar to those caused by planting severely diseased seed, but the two sources of inoculum had contrasting effects on plants from non-sprouted and sprouted seed. If the severity of stem canker is inversely related to the speed of shoot emergence (Harrison, 1978), it was to be expected that the disease would be more severe when the seed was not sprouted than when it was. This expectation was fulfilled on plants from seed with black scurf but the reverse occurred when inoculum was applied at planting, especially on King Edward in 1982 when stem canker was most severe on plants from sprouted seed. Many shoots were pruned off and further shoots were induced to develop, so contributing to the severity of disease, but i t is not known why this occurred most on plants from sprouted seed. Furthermore, in current investigations (unpublished), much more stem canker developed on shoots that emerged quickly from warm or dry soil than when emergence was delayed by cool or wet conditions, results that seem at variance with current ideas. It is apparent that the relationships between rate of shoot growth, disease and environment are not fully understood.

R E F E R E N C E S

BOGUCKA, H. z. (1978). Variation among Polish potato cultivars in susceptibility to Rhizoctonia solani and some factors influencing disease severity. Proceedings of the 7th Triennial Conference of the European Association for Potato Research, pp. 23 1-232.

BRENCHLEY, G. H . & WILCOX. H. J. (1979). Potato Diseases. H.M.S.0. London, 106 pp. F R A N K , J . A . (1978). The Rhizoctonia disease of potatoes in Maine. American Potato Journal 55, 59. G I G A N T E . R . (1969). Rhizoctonia solani infections in the potato tubers. Proceedings ofthe 4th Triennial

GLENDENNING. D. (1 965). Some aspects of the infection of potato stolons by Rhizoctonia solani. European

GRIFFITH. R . L. (1984). Effects of planting date on the development of stem canker (Rhizoctonia solani) Proceedings of the 9th Triennial Conference of the European

HARRISON, M . D. (1978). The Rhizoctonia disease of potatoes: importance and control. In Control of

H I D E , G. A. & CAYLEY, G. R. (1982). Chemical techniques for control of stem canker and black scurf

H I D E , G. A., READ. P. J. & SANDISON, J . P. (1985). Stem canker (Rhizoctonia solani) of maincrop potatoes.

Conference of the European Association for Potato Research, p. 197.

Potato Journal 8, 189-190.

in relation to early tuber yield. Association for Potato Research, pp. 109-1 10.

important fungal diseases ofpotatoes, pp. 129-1 50. Lima: International Potato Center.

(Rhizoctonia solani) disease of potatoes. Annals of Applied Biology 100, 105-1 16.

1 I . Effects on growth and yield. Annals of Applied Biology 106, 423-431.

422 G A H I D E . P . J R E A D A N D J . 4 Y E T P S A h D I S O N

MXXL.K. u' I (1978). The Rhizoctonia disease of potatoes: description and introductory observations in

S~DO\VSI( I . s di ZAWISLAK. I( (1975). Rhizoctonia solani Kiihn in monoculture of potato. Biuletyn

c .\\ I:UDF\, I H. (1965). Rhizoctonia solmi; results of recent experiments. European Potato Journal

Michigan. Anierican Potato Journal 55, 5 5 .

Insfj~trtru Zienzniaka 16, 89- 101.

8, 158-159.

(Received 7 August 1984)