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#flffin,ltrearer ?Ee"_w+ Rhizoctonia stem canker and black scurf of potato Phillip Whartonl, William Kirkl, Devan Berry1 and Sieglinde Snapp2 lDepartment of Plant Pathology, 2Department of Crop & Soil Sciences, Michigan State University Rhizoctonia stenn canker and black scurf economically significant damage only in cool, wet Rhizoctonia solani Kuhn soils. ln the more southern temperate areas of (Deuteromycetes, Mycelia Sterilia) Michigan, losses f rom Rhizoctonia are sporadic and occur only when the weather is cold and wet in the Introduction weeks following planting. In northern areas, where Rhizoctonia diseases of potato are caused by the growers often must plant in cold soils, Rhizoctonia fungus Rhizoctonia solani Kuhn (teleomorph Thana- is a more consistent problem. Poor stands, stunted plants, number and size, and mis- tephorus cucumeris [A. B. Frank] Donk) and can be reduced tuber found on all underground parts of the plant at various shapen tubers are symptoms of R. solaniinfection. times during the growing seas on. Rhizoctonia solani has many synonyms and is divided into subgroups Symptonns called anastomosis groups (AGs), in which isolates The symptoms of the disease are found on both are categorized according to the ability of their above- and belowground portions of the plant. hyphae to anastomose (fuse) with one another. Three Black scurf (Fig. 1) is the most conspicuous sign of AGs of R. solaniare prevalent in Michigan. AG2-2, Rhizoctonia disease. ln this phase of the disease, AG-3 and AG-4. AG-3 is the causal agent of disease the fungus forms dark brown to black, hard masses in potato; AG2-2 and AG-4 cause sugar beet crown on the surface of the tuber. These are called sclerotia and root rot and seedling damping-off, respectively. and are resting bodies of the fungus (Fig. 1). Sclerotia Rhizoctonia solani AG-3 is relatively specific to are superficial and irregularly shaped, ranging from potato, and sclerotia on tubers belong almost exclu- sively to AG-3. Other AGs of R. solani, such as AG2- 2 and AG-4, may be pathogenic to potato at some temperatures, but they generally cause little damage. ln Michigan, R. solanicauses black scurf on tubers (Fig. 1) and stem and stolon canker on underground stems and stolons (Fig . 2), and it occurs wherever potatoes are grown. However, R. solanicauses $ t1 "v Figure 1. Rhizoctonia solanisclerotia on the surface of Figure 2. Brown, sunken lesions on underground tubers. stems and stolons are caused by R, solani. fi$urltltnl,i.'l'.i,*,'.,',.,'..,;.'.ij''.''i'lil-..i Figure 3. Germinating sprouts may be killed by R. solani Figure 4. Small aerial tubers may form aboveground if before they emerge from the soil. stolons and underground stems are severely infected. small, flat, barely visible blotches to large, raised Stolons and roots can also be infected by R. solani. lumps. Although these structures adhere tightly to Early in disease development, stolons, roots and the tuber skin, they do not penetrate or damage the stems have reddish brown to brown lesions. As red tuber, even in storage. However, they will perpetuate to brown lesions mature, they become cankers that the disease, and if infected tubers are used as seed, are rough and brown and can have craters, cracks or inhibit the establishment of potato plants. both. Damage varies and can be limited to a superf i- cial brown area that has no discernible effect on plant Although black scurf is the most noticeable sign growth to severe lesions that are large, sunken and of Rhizoctonia, stem canker (Fig. 2) is the most necrotic. lf cankers are severe, they may girdle the damaging component of the disease. lt occurs under- stem, interfering with the normal movement of water ground and often goes unnoticed. Early in the season, and carbohydrates throughout the plant. the fungus attacks germinating sprouts underground before they emerge from the soil (Fig. 3). Sprouts Late-season damage to plants is a direct result of may be killed outright if lesions form near the growing cankers on stolons and stems causing problems tip (Fig. 3). Damage at this stage results in delayed with starch translocation. Stolon cankers also affect emergence and is expressed as poor and uneven the shape, size and numbers of tubers produced. stands with weakened plants. Reduction in crop vigor lf stolons and underground stems are severely results from expenditure of seed energy used to infected, the flow of starch from the leaves to the produce secondary or tertiary sprouts to compensate developing tubers is interrupted. This results in for damage to primary sprouts. Occasionally, heavily small, green tubers, called aerial tubers, forming on infested potato seed tubers are unable to produce the stem above the soil (Fig. 4). Formation of aerial stems. lnstead, the tubers will produce stolons with tubers may indicate that the plant has no tubers several small tubers. This symptom, referred to as of marketable quality belowground. lnterruptions "no top", can be confused with the same symptom in carbohydrate flow may also result in a stunting caused by physiologically old seed that has been or rosetting of the plant. A leaf curl, which can be desprouted. confused with symptoms of the potato leaf roll virus, has also been reported in severely infected plants. Poor stands may also be mistaken for seed tuber decay caused by Fusarium or soft rot bacteria unless Disease cycle plants are dug up and examined. Rhizoctonia does Rhizoctonia diseases are initiated by seed-borne or not cause seed decay, damaging only sprouts and soil-borne inoculum. The pathogen overwinters as stolons. Poor stands and stunted plants can also be sclerotia and mycelium on infected tubers, in plant caused by blackleg, a bacterial disease that origi- residue or in infested soils (Fig. 5). When infected nates from seed tubers and progresses up stems, seed tubers are planted in the spring, the fungus causing a wet, sometimes slimy rot. ln contrast, grows from the seed surface to the developing Bhizoctonra lesions are always dry and usually sunken. Early in season, SUMMER white mycelium often develops on plant parts in close contact with soil. This is the sexual stage of the fungus. Its role in the disease is not well known. LATE SUMMER/ When oberved, stem -> lesions are often FALL severe. Late-season damage may Roots and stolons may be resull in formation of attacked anytime during aerial tubers. the growing season. Mycelia and sclerotia on infected tubers infect Rhizoctonia solani developing sprout, root Disease Cycle and stolon primordia, " often nipping off growing tips. SPRING Sclerotia start to form on tubers when still attached to mother plant, and this continues into storage. q FALL lnfected seed and volunteer potatoes. Pathogen overwinters as sclerotia and mycelia on infected tubers, in plant residue or in infested soil. WINTER Figure 5. The disease cycle of the stem canker and black scurf pathogen, Rhizoctonia solani. sprout, and infection of root primordia, stolon primordia tively correlated with the temperature that is most and leaf primordia can occur. Seed-borne inoculum favorable for pathogen growth. The temperature is particularly effective in causing disease because of range for the growth of F. solaniAG-3 is 41' to its close proximity to developing sprouts and stolons. 77"F, so plants will be most susceptible to infection when the soil temperatures are within this critical Mycelia and sclerotia of R. solaniare endemic to range. Cool temperatures, high soil moisture, fertility Michigan soils, living on organic debris, and can and a neutral to acid soil (pH 7 or less) are thought cause disease independently of or in conjunction with to favor development of Rhizoctonia diseases of seed-borne inoculum. Soil-borne inoculum is poten- potato. Damage is most severe at cool temperatures tially as damaging as seed-borne inoculum, but it can because of reduced rates of emergence and because cause infection only when the plant organs develop growth of stems and stolons is slow relative to the in proximity to the inoculum. Roots and stolons may growth of the fungus. Wet soils warm up more slowly be attacked anytime during the growing season, than dry soils. This exacerbates damage because although most infections probably occur in the early excessive soil moisture slows plant development and part of the plant growth cycle. The plant's resistance favors fungal growth. lt has been shown that high soil to stolon infection increases after emergence, even- temperatures, especially during the early stages of tually limiting expansion of lesions. plant development, tend to minimize the impacts of R. solani, even when inoculum is abundant. Previous research has shown that soil temperature is a critical factor in the initiation of Rhizoctonia Sclerotia begin to form late in the season, principally disease in potato, with disease severity being posi- after vine death. The mechanisms involved in scle- rotial development on daughter tubers are different sclerotia are visible on one side of washed tubers, from those acting in the infection of the mother plant. consider using a different seed source. Tuber The mechanisms that trigger sclerotial formation are inoculum is more important than soil inoculum as the not well understood, but they may involve products primary cause of disease. Seed growers should plant related to plant senescence. However, daughter only sclerotia-free seed. tubers produced from infected mother plants do not always become infested with sclerotia. Following practices that do not delay emergence in the spring minimizes damage to shoots and stolons Monitoring and control and lessens the chance for infection. Planting seed Currently, it is not possible to completely control tubers in warm soil (above 46'F) and covering them Rhizoctonia diseases, but following a combination with as little soil as possible speeds sprout and stem of cultural and crop protection strategies may limit development and emergence, and reduces the risk their severity.