Rhizoctonia solani

Pathogen profile created by Paulo Ceresini
as one of the requirements of the course PP-728 Soilborne Plant Pathogens, offered on Spring 1999



Introduction
Rhizoctonia solani, the most widely recognized species of Rhizoctonia was originally described by Julius Kühn on potato in 1858. Rhizoctonia solani is a basidiomycete fungus that does not produce any asexual spores (called conidia) and only occasionally will the fungus produce sexual spores (basidiospores). In nature, R. solani reproduces asexually and exists primarily as vegetative mycelium and/or sclerotia. Unlike many basidiomycete fungi, the basidiospores are not enclosed in a fleshy, fruiting body or mushroom. The sexual fruiting structures and basidiospores (i.e. teleomorph) were first observed and described in detail by Prillieux and Delacroiz in 1891. The sexual stage of R. solani has undergone several name changes since 1891, but is now known as Thanatephorus cucumeris.


Host range and distribution

R. solani  is a very common soilborne pathogen with a great diversity of host plants. The Table 1 illustrates the relationship of particular anastomosis groups of R. solani  and the hosts they infect.


Isolation

Qualitative determinations of R. solani in infected plants are made by isolations from infected host plant tissues. Infected plant tissues are cut in pieces of 5 cm, washed in running tap water to eliminate any attached organic debris, and blotted to dry. Small samples of plant tissue (0.5 cm of length) are then cut from the lesions and transferred to an isolation medium, which can be either general (e.g. alkaline water agar) or selective (e. g. modified Ko & Hora medium). The alkaline water agar medium provides a faster way of isolating the fungus than other general media since successful isolation of R. solani can be obtained after 24 h of transfer (Guttierrez et al., 1997).

Quantitative determination of R. solani from soils to estimate the inoculum density are based on the saprophitic and/or pathogenic competitive abilities of the fungus. Methods developed from this principle included the burial and subsequent recovery of various substrates as baits for Rhizoctonia. The baits include suscetible host plants, autoclaved seeds, stem segments such as flax, buckwheat, bean, cotton and cereal straw, and even agar baits. Other methods include different soil sieving procedures combined with selective media for the isolation of R. solani from soil. A subsequent method using a multiple-pellet soil-sampler was developed for quantitative estimation of propagule density of R. solani based on placement of weighed amounts of soil, or soil pellets on water agar supplemented with chloramphenicol, or on selective media (Hennis et al. 1978, Ko & Hora 1971, Castro et al. 1988).


Identification

The vegetative mycelium of R. solani and other Rhizoctonia fungi are colorless when young but become brown colored as they grow and mature. The mycelium consists of hyphae partitioned into individual cells by a septum containing a dough-nut shaped pore. This septal pore allows for the movement of cytoplasm, mitochondria, and nuclei from cell to cell. The hyphae often branch at a 90o angles and usually possess more than three nuclei per hyphal cell. The anatomy of the septal pore and the cellular nuclear number (CNN) have been used extensively by researchers to differentiate R. solani from other Rhizoctonia fungi. R. solani [renamed Moniliopsis solani = Moniliopsis anderholdii (Moore, 1987)] is characterized by: CNN close to the tips in young hyphae greater than two, main runner hyphae usually wider than 7mm, mycelium buff-colored to dark brown, sclerotia (if present) irregular shape, light to dark brown, not differentiated into rind and medula and having Thanatephorus cucumeris its as teleomorph.

Because R. solani and other Rhizoctonia fungi do not produce conidia and only rarely produce basidiospores, the classification of these fungi often has been difficult. Prior to the 1960ís, researchers relied mostly on differences in morphology observed by culturing the fungus on a nutrient medium in the laboratory and/or pathogenicity on various plant species to classify Rhizoctonia. In 1969, J. R. Parmeter and his colleagues at the University of California in Berkeley, reintroduced the concept of "hyphal anastomosis" to characterize and identify Rhizoctonia. The concept implies that isolates of Rhizoctonia that have the ability to recognize and fuse (i.e. "anastomose") with each other are genetically related, whereas isolates of Rhizoctonia that do not have this ability are genetically unrelated.

Anastomosis groups of binucleate and multinucleate Rhizoctonia spp.

Hyphal anastomosis criteria have been used extensively to place isolates of Rhizoctonia into taxonomically distinct groups called anastomosis groups. In practice, hyphal anastomosis is determined in several ways. The most commonly employed practice involves pairing two isolates of Rhizoctonia on a glass slide and allowing them to grow together. The area of merged hyphae is stained and examined microscopically for the resulting hyphal interaction(s).

Pairing of isolates belonging to the same AG-results in hyphal fusion (anastomosis), leading to either acceptance (self-pairings) or rejection (somatic incompatibility). Pairings between AGs do not result in hyphal fusion, suggesting greater genetic differences between isolates (i.e., different species, etc.) Interpretation of anastomosis reaction is not always straightforward because the four hyphal interaction phenotypes (C0 to C3) represent a continuum.  Within an AG, two types of hyphal interactions (C2 and C3) are most relevant for the study of population biology. The C2 reaction (also referred as killing reaction), represents a somatic incompatibility response between genetically distinct individuals. The C3 reaction (perfect fusion) between two isolates is indicative of genetic identity or near identity.

Very little is known about the genetic mechanisms controlling this recognition process in Rhizoctonia. In other filamentous fungi, somatic incompatibility is controlled by several genes with multiple alleles. For two fungal isolates to be compatible, all somatic compatibility loci must be the same.

Isolates of R. solani have been assigned to 12 AGs. Recent protein and DNA-based studies support the separation of R. solani into genetically distinct groupings, but has also revealed considerable genetic diversity within an anastomosis group. Hyphal anastomosis and molecular methods are currently being used to further examine the taxonomy, ecology and pathology of R. solani.


Symptoms

R. solani primarily attacks below ground plant parts such as the seeds, hypocotyls, and roots, but is also capable of infecting above ground plant parts (e.g. pods, fruits, leaves and stems). The most common symptom of Rhizoctonia disease is referred to as "damping-off" characterized by non germination of severely infected seed whereas infected seedlings can be killed either before or after they emerge from the soil. Infected seedlings not killed by the fungus often have cankers, which are reddish-brown lesions on stems and roots. In addition to attacking below ground plant parts, the fungus will occasionally infect fruit and leaf tissue located near or on the soil surface. This type of disease often occurs because the mycelium and/or sclerotia of the fungus are close to or splashed on the plant tissue.

Although most Rhizoctonia diseases are initiated by mycelium and/or sclerotia, several important disease of beans, sugar beet, and tobacco result from basidiospore infection.These basidiospores also serve as a source for rapid and long distance dispersal of the fungus. The basidiospores germinate to produce hyphae that infect leaves during periods of high relative humidity and periods of extended wet weather. Under these conditions, basidiospores can often be observed on the base of stems near the soil surface or on the underside of leaves in the plant canopy.


Ecology and life cycle

R. solani can survive for many years by producing small (1 to 3-mm diameter), irregular-shaped, brown to black structures (called sclerotia) in soil and on plant tissue. Certain rice pathogens of R. solani, have evolved the ability to produce sclerotia with a thick outer layer that allows them to float and survive in water. R. solani also survives as mycelium by colonizing soil organic matter as a saprophyte, particularly as a result of plant pathogenic activity. Sclerotia and/or mycelium present in soil and/or on plant tissue germinate to produce vegetative threads (hyphae) of the fungus that can attack a wide range of food and fiber crops.

The fungus is attracted to the plant by chemical stimulants released by actively growing plant cells and/or decomposing plant residues. As the attraction process proceeds, the fungal hypha will come in contact with the plant and become attached to its external surface. After attachment, the fungus continues to grow on the external surface of the plant and will causes disease by producing a specialized infection structure (either an appresorium or infection cushion) that penetrates the plant cell and releases nutrients for continued fungal growth and development. The infection process is promoted by the production of many different extracellular enzymes that degrade various components of plant cell walls (e.g. cellulose, cutin and pectin). As the fungus kills the plant cells, the hyphae continues to grow and colonize dead tissue, often forming sclerotia. New inoculum is produced on or in host tissue, and a new cycle is repeated when new substrates become available.


Links to other sites

Rhizoctonia research
Rhizoctonia Diseases on Potato
Rhizoctonia Sheath Disease Complex in Rice
Rhizoctonia Root Rot on Wheat
Rhizoctonia Diseases on Lettuce
Dry bean diseases
Availability of germplasm for resistance against Rhizoctonia spp.  (USDA)
Rhizoctonia on corn


Acknowledgements

We acknowledge Drs. Marc Cubeta, David Shew and Gloria Abad for supplying us with a series of slides to illustrate the host range of R. solani. Special thanks also for Heather Hartzog for drawing the life cycle of the pathogen.


Selected references

  • Adam, G. C. 1988. Thanatephorus cucumeris (Rhizoctonia solani) a species of wide host range. In Advances in Plant  Pathology, Vol. 6. Genetics of Plant Pathogenic Fungi. (G.S. Sidhu, ed.), pp. 535-552. Academic Press, New York.
  • Agrios, G. N. 1997. Plant Pathology. 4th Ed., 606 pp. Academic Press, New York.
  • Alexopoulos, C. J., Mims, C. W. and Blackwell, M. 1996. Introductory Mycology.,  4th Ed., 869 pp., John Wiley  and Sons, New York.
  • Anderson, N.A. 1982. The genetics and pathology of Rhizoctonia solani. Ann. Rev. Phytopathol. 20:329-347
  • Castro, C., Davis, J. R., and Wiese, M.V. 1988. Quantitative estimation of Rhizoctonia solani AG-3 in soil. Phytopathology 78:1287-1292.
  • Cubeta, M.A., and R. Vilgalys. 1997. Population biology of the Rhizoctonia solani complex. Phytopathology 87:480-484.
  • Guttierez, W.A., H.D. Shew, and T. A. Melton. 1997. Sources of inoculum and management for Rhizoctonia solani damping-off on tobacco transplants under greenhouse conditions. Plant Disease 81:604-606.
  • Hawksworth, D. L., Kirk, P. M., Sutton, B. C., and Pegler, D. N. 1995. Ainsworth and Bisbyís, Dictionary of the  Fungi. 8th Ed.,  616 pp. University Press, Cambridge, UK.
  • Hennis, Y., Ghafar, A., Baker, R. and Gillespie, S.L. 1978. A new pellet soil sampler and its use for the study of population dynamics of Rhizoctonia solani in soil. Phytopathology 68: 371-376
  • Ko, W. H., and Hora, F. K. 1971. A selective medium for the quantitative determination of Rhizoctonia solani in soil. Phytopathology 61:707
  • Ogoshi, A. 1987. Ecology and pathogenicity of anastomosis and intraspecific groups of Rhizoctonia solani Kühn. Ann. Rev. Phytopathol. 25:125-143.
  • Sneh, B., Burpee, L., and Ogoshi, A. 1991. Identification of Rhizoctonia species.133pp. APS Press, St. Paul, MN, USA.
  • Sneh, B., Jabaji-Hare, S., Neate, S. and Dijst, G. 1996. Rhizoctonia species: Taxonomy, Molecular Biology, Ecology, Pathology, and Control, 578 pp. Kluwer Academic Publishers, Dordrecht, The Netherlands.
  • Vilgalys, R., and M. A. Cubeta. 1994. Molecular systematics and population biology of Rhizoctonia. Annu. Rev. Phytopathol. 32:135-155

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