Epidemiology: Management of Rhizoctonia Diseases of Potato

Introduction

It is difficult to overemphasize the role of potato (Solanum tuberosum L.) in the world’s food economy. Potato has very great diversity and contributes to global food security, delivering more abundant starch on a hectare basis than any other edible crop. The constant failure of cereals to meet both local and international demands coupled with the rapid increase in food prices has increased the demand for potato, which is highly nutritious and easily grown. Gibson and Kurilich also postulated that potato is very nutritious as it serves as a good source of carbohydrates, high-quality proteins, vitamins, and minerals. According to Fernandes et al. 2005, it was found that potato has little fat, as well as phytochemicals, such as carotenoids and natural phenols. Ncobela et al. (2017), also suggested that the potato crop could be used in livestock feeding, fuel production, and industrial purposes. Similarly, Pedreschi et al. (2008), reported that almost 50% of the overall potato produced are been utilized in the manufacturing industry with over 70% of tubers used as chips and French fries in the US. Furthermore, Friedman (2006), reported that potato tubers contain numerous secondary plant metabolites which are useful components of the human diet. Potatoes also have beneficial health characteristics and increase glucose tolerance and sensitivity to insulin. It also decreases the concentrations of plasma cholesterol and triglycerides and thereby increasing lipid profiles and reducing the risk of infection (Carla et al., 2013). It is, therefore, not surprising that better attention has been given to potato production in recent years.

Plant-parasitic fungi produce phytotoxins to initiate disease infection. For instance, Rhizoctonia solani produces a large number of hydrolytic enzymes including cellulases, pectinases, xylanases, and proteases (Olivieri et al., 2004), resulting in maceration of tissue and death of cells (Alghisi and Favaron, 1995). These dead tissues serve as the nourishing resource of the pathogen (Aveskamp et al., 2008). There is limited information on the function of phytotoxins in the growth and development of plants or in Rhizoctonia disease.

The management of the disease with synthetically derived pesticides has many side effects, such as pollution of underground water bodies and the environment. The indiscriminate misuse of these pesticides has also led to severe harmful effects on humans (Shoda, 2000) and plant chemical resistance growth. The increasingly harmful effects of synthetic pesticides and the development of chemical resistance by several plant pathogens have necessitated the development of alternative control strategies. This is to prevent the increasing shortfalls in annual crop productivity within the global agricultural sector, which consequently threatens global food security. This is crucial towards the introduction of integrated strategies to minimize the negative impact of excessive application of synthetic chemical-based products. Because phytotoxins are bioactive compounds, several studies have attempted to exploit its applications. Buiatti and Ingram (1991) recommended some phytotoxins as potential markers for screening disease-resistant plants due to their role in disease development. Also, Strobel et al. (1991) suggested that phytotoxins could be used as potential herbicide since they are toxic not only to crop plant but also to weeds and herbs. Phytotoxins are thought to play an important role in microbes entering plant tissues. In the final analysis, knowledge of the function and mechanisms of phytotoxin production, mode of activity, and their interactions with plant defense mechanisms will contribute to the creation of effective techniques to increase plant resistance to fungal pathogens. The review will be beneficial to crop producers as it will complement efforts to control the disease effectively.

Rhizoctonia diseases of potato

The most harmful disease in potato production is the black scurf and stem canker potato disease caused by the soil-borne fungus Rhizoctonia solani Kühn (teleomorph: Thanatephorus cucumeris (Frank) Donk) (Kara and Arici, 2019). R. Solani does not develop asexual spores, but survives as sclerotia (dense asexual hyphal resting structures), mycelium (hyphal growth form), or asidiospores (Ajayi-Oyetunde and Bradley, 2018). Sclerotia from R. Solani are compact bodies of deposited melanized hyphae that are immune and help the pathogen survive for long periods under extremely serious conditions (Abbas et al., 2019). In potato-growing areas, the disease is popular. In temperate climates, however, its magnitude is higher than in the tropics. The disease causes the crop to suffer both quantitative and qualitative economic harm. Quantitatively, losses occur due to stem, stolon, and root infection, which decreases tuber size and number, whereas qualitative losses occur because the disease is frequently associated with malformed tubers and black scurf discolorations. Rhizoctonia solani does not only affect potatoes but the disease has destructive effects on many plants, including Rice, Maize, Wheat, Lettuce, Sugar beet, Cotton, Alfalfa, Peanuts, Soybeans (Ajayi-Oyetunde and Bradley, 2018), and Cowpea (Kankam et al., 2018). Stem canker is promoted by cool temperature as it delays emergence after planting. Isakeit (2011) postulated that non-infected seed tubers could be planted and potatoes could be rotated for 1-2 years in other to prevent and manage stem canker disease that causes a considerable effect on potato plants.

Rhizoctonia disease cycle and disease symptoms

Potato Rhizoctonia diseases can be divided into two phases: cankers of Rhizoctonia, which are lesions of underground plant organs that can occur at any time during plant growth; and sclerotia deposition on the surfaces of tubers (Kara and Arici, 2019). The source of inoculum begins the life cycle of R. solani. Mycelia or sclerotia, present in soil or rotting plant matter in the field, or on the surfaces of seed tubers, maybe the inoculum source (Johnson and Leach 2020). The pathogen may occur saprophytically during mycelial development or can infect potato roots, stems, stolons, and tubers that develop. Brown to black sunken lesions are seen on sprouts, stolons, or roots shortly after plant emergence. These lesions may cause stem girdling, resulting in wilting and death.

Infection cushions on the surfaces of the host sprouts and roots are created by the pathogen, and penetration by the pathogen only takes place under favorable conditions in these areas. Lesions then mature and enter the vascular bundles under the infection cushions, where they develop into the symptoms of the 'canker'. Also, sprout-nipping a phenomenon whereby lesions girdle and kill young sprouts may occur (Johnson and Leach, 2020), and lead to poor plant emergence and sparse rooting in affected crops. Aerial tubers, upward leaf roll, chlorosis, and pigmentation of the purple leaf can be above-ground symptoms (Coca Morante, 2019). The infection process may occur, destroy or cause malformation and the 'cracking' of tubers on newly formed stolons.

Sclerotia grows on the daughter tubers (black scurf) at the end of the growing season, which is the most visible symptom. Among the anastomosis groups, AG-3 is the only member that is proven to cause an increased prevalence of black scurf on daughter tubers of potato (Woodhall et al., 2008). If the pathogen progresses into the sexual stage, a ‘white-collar’ generating basidiospores develop on stems just above the soil surface, but only AG3s are seen to undergo this stage on potatoes (Woodhall et al., 2008).

The yield effect on the potato variety by Rhizoctonia diseases depends on the R. solani strains, the potato cultivar, and environmental conditions. It was shown by Otrysko and Banville (1992) that R. solani AG-3 dramatically reduced overall and sellable crop yields and improved potato black scurf yields. It was also found by Hartill (1989) that R. solani infection resulted in a rise in the number of tubers attacked, as well as tubers growing on leaf axils, suggesting that stolon cankers obstruct the transport of photosynthetic products. Infection of tubers by R. Solani AG-3 was detected to be the source of dark skin spots on stored tubers prior to skin setting due to the deposition of the waterproofing waxy material in the tuber reaction.

Anastomosis groups of R. solani

Historically speaking, R. Solani, based on anastomosis reactions, was subdivided into subsets. It is dual-plated with tester isolates to establish the group of a new isolate and whether there is a merger between the hyphae of the two isolates, including a 'death zone' around the fusion, they are placed into the same group of anastomosis (AG) (Gondal et al., 2019). At present, 14 Rhizoctonia AGs have been identified, with so many subgroups based on a broad variety of characteristics, such as host range, virulence, molecular and biochemical features, and morphology (Samsatly et al., 2018; Kouzai et al., 2018; Picarelli et al., 2019). Together with other molecular and biochemical instruments, the advent of Polymerase Chain Reaction and rDNA sequencing has identified the genetic diversity of AGs. (Yang et al. 2017).

According to Muzhinji et al. (2015), strains of AGs 3, 1, 2-1, 9, 4, and 5 are economically important for potatoes in temperate climates across the globe while several isolates of R. solani AGs are related to underground potato organs. AG-3 is the most cosmopolitan group exhibiting disease symptoms in potatoes (Ito et al. 2017). The AG-3 subgroup is further divided into two subgroups with non-overlapping host ranges. AG 3 PT strains are virulent on potatoes, whilst AG 3 TB is virulent on tobacco (Ito et al. 2017). Wibberg et al. (2017) postulated that sexual spores of R. solani cause leaf lesions on potatoes, even though the functioning of basidiospores in disease etiology is not well understood. Date et al. (1984) also documented that R. solani AG-3 cause tomato foliar blight in Japan. Members of R. solani strains that are pathogenic to potatoes are non-obligate, and saprophytes that can consume a wide range of substrates. Though members of AG-3 are widely reported by many researchers to be linked with potato plants, isolates seen in potato fields in Maine were of diverse anastomosis groups (Bandy et al., 1984).

Effective functioning, nutrient transportation, and signaling of molecules within the colony are dependent on hyphal fusions in higher fungi. The fungus must have the capacity to target and recognize other hyphae in order for this process to occur. Hyphae prevent each other in a normal system in order to maintain a radiating, exploratory hyphal network. Anastomosis reactions, however, may be caused by environmental factors, especially nutrients. According to Carling (1996) R. solani, is known to influence anastomosis by the amount of available nutrients, particularly nitrogen.

Epidemiology of R. solani

Potato plants' soil-borne pathogens, such as R. Solani are popular in all regions of the world growing potatoes and have also invaded several plant species (Abdoulaye et al., 2019). This is due to the fact that the pathogens are distributed on seed tubers as potatoes are propagated vegetatively. Infection attributable to R. Solani can result from inoculum, either tuber-borne or soil-borne (Abdoulaye et al., 2019). The primary cause of infection is tuber-borne inoculum in organic potato development. Penetration and infection mode by R. Solani is well studied by numerous scholars. The mechanisms of infection and penetration depend largely on the isolate, anastomosis classes, plant organisms, and the nature of the plant parts formation (Murray, 1982).

R. Solani has reduced movement due to a lack of spores and persists in harsh environments by the development of sclerotia or latent mycelia (Johnson and Leach, 2020) that can live for many years in plant residues and soil (Šišić et al. 2018). Peters et al. (2003) stated that in the absence of host plants, the inoculum levels are lower as R. solani population declines with time leading to more years between potatoes cropping. A wide range of crops including carrot, eggplant, radish, and oats have been reported as alternative hosts to R. solani of AG-3 via the development of epiphytic connections with these crops (Carling et al., 1986). The development of hyphae and sclerotia on other alternative crops makes the selection of crops for rotation key in potato production. In conditions that delay the growth of new shoots, especially in cold, moist soils, and acid-to-neutral soils, Rhizoctonia disease is prevalent (Johnson and Leach, 2020). AG-3s have been found to cause more harm at 10 ° C or low temperatures to potato plants than at higher temperatures (Johnson and Leach, 2020), and temperatures above 25 ° C have been shown to inhibit the severity of canker (Anderson, 1982).

Phytotoxins

Phytotoxins are microbial secondary metabolites produced by a pathogen in culture or in infected plant tissues which are toxic to plants. Thus, microbial toxins are toxic secondary metabolites produced by fungal species. During the invasion of plant tissues by microbes, these metabolites are produced to enable them to penetrate and colonize the plant tissues.

Chemical structures of phytotoxins

The chemical structure of phytotoxins varies from simple molecules to relatively complex molecules. Whilst Liang and Zheng (2012) isolated polyketide-based lactones from the genus Rhizoctonia, Pedras et al. (2005) isolated complex cyclic peptides demonstrating the wide variety of chemical configurations of phytotoxins. Phenylacetic acid (1) and hydroxy (2-3) and methoxy (4) derivatives of PAA, benzoic acid (5), and Nb-acetyltryptamine (6) plant growth regulator synthesis have been reported as essential metabolites of R. Solani infection processes on different plants (Hu et al., 2018). Other scholars have also described most carboxylic acids, including PAA and MeO-PAA, as phytotoxins exhibiting non-specific action against rice. (Liang and Zheng, 2012). Kankam et al. (2016a) also isolated toxic compounds such as 3-methylthiopropionic acid (3-MTPA) and 3-methylthioacrylic acid (3-MTAA) which caused harm to potato plants as they trigger stem canker without the presence of R. Solani isolates (Kankam et al., 2016b). Additionally, secondary metabolites that are harmful to plants are produced by formae speciales of Fusarium oxysporum. It is suspected that they are important in the pathogenicity of wilted diseases. The toxins produced by these pathogens are fusaric acid created by F. oxysporum f. sp. cubense on banana and a polypeptide toxin produced by F. oxysporum f. sp. vasinfection on cotton (Thangavelu et al., 2001; Bell et al., 2003). Spore germination fluids of Aternaria brassicola are considered to be phytotoxic (Cook et al. 1997). In another analysis, the germination percentage of the seeds was decreased by 24 hours when soybean seeds were soaked in the fungal filtrates of Fusarium solani, Aspergillus niger, Alternaria terreus (Strobel, 1982; Ibraheem et al., 1987). This shows that phytotoxins were released into the media in which they were grown. Dong et al. (2012) also postulated that both crude toxin and pure fusaric acid isolated from Fusarium oxysporum f. sp. cubense race 4 produced disease symptoms on banana seedlings almost the same with those of pathogen infection. There is also one published report in maize, where only fumonisin-producing strains of Fusarium verticillioides caused disease symptoms on seedlings without the presence of the fungus, and that treatment with purified fumonisin alone was enough to produce the same symptoms (Williams et al., 2007).

Phytotoxins from Rhizoctonia solani and mechanism of action

Rhizoctonia solani may enter the host through mechanical means or with the aid of enzymes or toxins (Hu et al., 2018). The deleterious effect of phytotoxins produced by R. solani on plants cannot be overemphasized. For example, Lai et al. (1968) found in their studies that Rhizoctonia solani produces phytotoxins which may result in changes of permeability in infected cell membranes and the breakdown of the cell wall of Phaseolus aureus. Yoder (1980) has stated that one of the main factors involved in the growth of canker caused by R. solani is phytotoxin in seedlings of beans. Again, Wyllie (1962) postulated that the development of symptoms in host tissue before hyphal colonization could be due to the production of phytotoxic substances by R. solani. Phenylacetic acid (PAA), three hydroxy (OH-), and one methoxy (MeO-) derivative of (PAA) as produced by R. Solani is found to be crucial in the process of plant parasitism and infection (Hu et al., 2018). The role of PAA and its derivatives in plant growth-regulating activities and phytotoxicity on other plant species have been reported (Hu et al., 2018). However, in previous studies, conflicting findings and methodological limitations on the basic role of PAA in the production of Rhizoctonia disease and the optimum concentrations required to induce disease in their host are unclear (Betancourt and Ciampi, 2000). The role of OH- and MeO- derivatives of PAA in the growth and development of plants or Rhizoctonia disease is lacking. PAA has also been shown to have antimicrobial properties and to inhibit R. solani growth and this is contradictory to Ding et al. (2008) observations that the fungus develops and metabolizes PAA.

Lakshman et al., (2006) reported that derivatives of PAA such as PAA and the OH and MeO are absorbed by R. solani from phenylalanine via the pathway of shikimate. Hermann and Weaver (1999) indicated that this route includes two metabolic intermediates with the carbon metabolism pathway of quinic acid (QA), which is caused by the presence of QA in the growth substrate as it is discharged from lignin in the rotting plant material. The transition between the parasitic and saprobic phases of this fungus' life cycle can be regulated by the interaction of these metabolic pathways. The activation of the QA pathway has recently been shown to contribute to the sequestration of intermediates from the shikimate pathway, which reduces the development of the PAA precursor phenylalanine in R. Solani and other fungal filaments (Liu et al., 2003a). Liu et al. (2003b) have stated that it reduces the pathogenicity of R. solani when the metabolic processes within the fungus are disrupted by the addition of QA-containing substrates from host crops.

The management of Rhizoctonia disease of potato

R. solani disease management strategy aimed at altering fungal metabolism giving an innovative idea as existing practices such as the use of fungicides are essentially based on reducing fungus populations (Sweetingham, 1996). An expanded awareness of R. solani metabolism will result in the production of more successful and advanced disease suppression methods, thus enhancing the health of plants. The various control measures for Rhizoctonia potato disease include the following:

Biocontrol

For use as possible biocontrol agents, bacteria, fungi, and mycophagous soil fauna have all been tested (Bagy et al., 2019; Jiang et al., 2019). Rhizoctonia antagonistic bacteria such as Bacillus pp. (Schreiter et al., 2018) and Pseudomonas species (Yu et al., 2017) were successfully used as bioagents in Rhizoctonia disease management. Plant growth-promoting rhizobacteria (PGPR) that are closely associated with plant root systems have a net beneficial effect on plant health and were used for disease control (Gouda et al., 2018; Xiang et al. 2017b; Abbas et al., 2019). In addition to direct pathogen inhibition, rhizobacteria prevent Rhizoctonia diseases by inhibiting the development of pathogens in plant tissues, preventing the creation of parasite complexes, and enhancing plant defenses. Diallo et al. (2011) also confirmed that the potato rhizosphere has been widely colonized by Pseudomonas spp. in particular P. fluorescens and P. putida, and is heavily expressed in the root internal microenvironment. Several strains of Pseudomonas spp. are regarded as PGPR, which contributes to plant health either indirectly by reducing the development and/or activity of organisms detrimental to plant health or sequestering heavy metals (Van Loon and Glick, 2004). The combination of required physical niche and biocontrol ability makes members of the Pseudomonas genus great contenders for the regulation of Rhizoctonia diseases.

Most of the Bacillus spp. Inclusive B. subtilis, B. thurigiensis, and B. cereus have been described as effective methods to manage Rhizoctonia disease (Abbas et al., 2019; Madhavi et al. 2018). Strains from many Bacillus species are again proven to help cause mediated systemic resistance in a number of plant species and provide defense against Rhizoctonia disease (Mekonnen and Fenta, 2020). Gururani et al. (2013) found that when plant growth promoters of rhizobacteria are embedded in potato field soils, they increase the resistance of abiotic stress in the crop by triggering changes in the expression of ROS-scavenging enzymes and by stimulating photosynthetic efficiency. Tomilova et al. (2020) have also found that the use of B. bassia for the treatment of potato tubers before planting decreased Rhizoctonia infection in potato stolon and stems. Commercialized biopesticides like Botrycid, Sublic, and Rhizo Plus have been reported to be potent against Rhizoctonia solani (Abbas et al., 2019). Below are bioactive compounds with antimicrobial properties against Rhizoctonia solani.

Cultural practices

Cultural practices are the most widely recommended and utilized option in managing disease incidence in several places of the world (Katan, 2010). These include; (i) crop rotation (ii) field sanitation by elimination of diseased potato plants, (iii) fallow, (iii) flooding, (iv) weed control during the first 3 weeks of potato emergence, (v) crops with antagonistic effect, and (vi) the addition of organic amendments (Arici and Sanli, 2014).

Crop rotation is among the most efficient and less expensive management methods for farmers in developing countries (Bridge, 1996). Crop rotation has in many instances appeared to be beneficial in managing R. solani disease affecting potatoes worldwide as it can have overwhelming effects on crops grown in multiple consecutive years and decrease in inoculum levels due to the absence of preferred hosts (Larkin and Brewer, 2020). According to Adesiyan et al., (1990), susceptible crops are rotated with resistant or completely immune crops in crop rotation. Larkin et al. (2010) indicated in Canada that 2 –year cropping systems, it seemed that potatoes grown after red clover were showing less black scurf compared to potatoes grown after barley or Italian ryegrass. It is also recorded that ryegrass and barley rotation significantly reduced the incidence of Rhizoctonia disease in potatoes (Larkin and Brewer, 2020). The above report indicates that these crops are appropriate choices for crop rotation in disease control and management.

Among the several measures required for an efficient disease management strategy in the controlled environment and that of the field is sanitation. Sanitation involves any procedure that aims to discourage the transmission of plant diseases by eliminating diseased and asymptomatic contaminated tissue, as well as contaminating tools, equipment, and washing hands.

Antagonistic crops produce antihelminthic compounds (Grainge and Almed, 1988) which contain toxic substances that can destroy or kill fungal pathogens after plant invasion (Karban, 2011). Certain plants produce toxic exudates that directly kill fungi, whilst in other plants; fungi fail to complete their life cycle after the invasion of the plant tissue. Plants that exhibit this type of antagonism are often known as trap crops.

Chemical control

Chemical control comprises the application of botanical or organic synthetic compounds that have a killing, inhibiting, or repulsive effect on injurious organisms threatening mankind and animals (Oudejans, 1991). There is also a published report of disease management options against stem canker and other fungal diseases with the use of fungicides (Kataria et al., 1991). For example, Chen et al. (2019) indicated that seed-treated fungicides like Vertisan EC1.67, Elatus 45WG, Regalia 5SC, Priaxor 4.17SC, and Quadris 2.08SC were potent in controlling potato Rhizoctonia diseases. Similarly, Johnson et al. (2000) also postulated that when potato plants were treated with dimetomorph, propamocarb, and cymoxanil after disease infection, it considerably decreased the sporulation of Phytophthora infestans on plants.

However, there are no chemicals registered to control R. solani in potato, and chemical control for stem canker diseases is often expensive and not stable in the field. Isakeit (2011) reported that commercial growers can also use fungicides at planting, either to treat the seed tubers or as an in-furrow soil treatment against stem canker. The use of selective fungicides has been found to increase the resistance to Rhizoctonia solani. Several chemical products have been specifically developed to combat seed-borne potato diseases as well as provide broad-spectrum control for Rhizoctonia, Silver Scurf, and Fusarium Dry Rot diseases (Wharton et al., 2007). These chemical products include Quadris (a.i. azoxystrobin), Maxim 4FS (a.i. fludioxinil), Tops MZ (ai. thiophanate-methyl), and other Maxim formulations Mancozeb (Wharton et al., 2007). The general effect of these seed treatments and the in-furrow fungicides applied are recognized in the crop growth and crop vigor, but intermittently, the use of seed treatments in conjunction with cold and wet soils can contribute to delayed seed growth (Wharton et al., 2007).

Study goals call for new methods of defense that are consistent with sustainable cultivation, thus promoting the usage of complementary methods, such as the use of bio-organic fertilizers in the management of stem cankers (Diallo et al., 2011). Fungicides pose problems in areas of low rainfall. For instance, in regions where planting dates must coincide with rainfall, fields are often too dry to be treated effectively before the rains come. However, the effectiveness of these chemicals depends on the time of application, climate, and knowledge of nematode population dynamics.

Over-reliance on the use of fungicides to control fungi increases production costs exposes farmers to toxic chemicals and reduces the efficiency of the chemicals. Moreover, certain microorganisms in the soil may develop resistance to the chemical and break it down to harmless products (Seong et al., 2017). Considering the numerous disadvantages of chemical control, and the limited possibility of its applications by small-scale farmers, the need for an alternative control is necessary.

Preformed defense systems

Plants possess many attributes which allow them to either resist infection or to withstand aggressive growth and feeding of pathogens (Nürnberger and Lipka, 2005). The existence of mechanical barriers such as fur, spikes, resins, and waxes on the cuticle, as well as thick cell walls on the plant surface, are the first defense barriers that pathogens must surpass in order for infection to occur (Nürnberger et al., 2004). These mechanical barriers prevent pathogen entry, while chemical defenses are triggered when they turn out to be defective (Nürnberger and Lipka, 2005).

An extensive range of secondary chemical compounds, which defend the host from pests and pathogens, are primarily exhibited in healthy plants, either in their active state or as inactive precursors ready to react when tissue integrity is compromised (Morrissey and Osbourn, 1999). The inhibitory effect of plant compounds such as catechols (Osbourn, 1996a) is so high that the inhibitory effect reaches the host surface from the initial point of synthesis, blocking pathogen development or repulsing pathogens and other pests (Osbourn, 1996a). However, in many instances, advanced pathogens can resist or even use these toxic chemicals as a reference to the host or as nutrients (Bennett and Wallsgrove, 1994; Osbourn, 1996b). Preformed inhibitors are generally located in cells immediately below the plant surface; within plant cell vacuoles and other organelles, and many are tissue-specific (Bennett and Wallsgrove, 1994). Bennett and Wallsgrove (1994) in their studies found that saponins, terpenoids, sugar-containing phenolic, phenols, sulfur-containing compounds, glucosinolates, and cyanogenic glucosides have antibiotic properties.

Biologically active secondary metabolites, including pepper, tomato, eggplant, and tobacco, are abundant in the Solanaceae. These poisonous metabolites also shield the plant from minor diseases and pests, such as herbivorous insects, and cause medical issues to animals, including humans, at large doses. The two most common glycoalkaloids in potatoes are α-chaconine and α-solanidine. Symbiotically, they prevent the growth and germination of many essential pathogenic fungi, including R. solani, when plants are grown under controlled conditions (Fewell and Roddick, 1997).

Organic matter amendments

Among the other management approaches mentioned, the application of organic modifications has been proposed by many mycologists. Research findings have proven that organic modifications are effective for controlling soil-borne fungal plant pathogens, including Rhizoctonia spp. (Arici and Sanli, 2014). According to Amadioha (2003), they are quickly degraded, and pollution-free; they leave no hazardous traces, are cheaper, and not dangerous to living organisms. In all cases, the materials are added to the soil in a dry or fresh state (Sikora and Fernàndez, 2005). Several studies have shown that the incorporation of selected organic matter amendments in biocontrol treatments has improved the inhibiting ability of either component alone. (Scheuerell et al., 2005; Pugliese et al., 2011). This confirms the theory that Rhizoctonia diseases are regulated by a limited number of soil microorganisms (Hoitink and Boehm, 1999). As a result, changes to organic matter can only eradicate these pathogens if they can sustain populations of suppressive species already found in soil or strains that are added simultaneously with the amendment.

The mechanisms by which suppressive agents control diseases are through competition with pathogens for nutrients (Raviv, 2008), the production of antibiotics harmful to pathogens (Craft and Nelson, 1996), and the activation of a plant defense response (systemic acquired resistance or induced systemic resistance) in plants (Nelson and Boehm, 2002). Phytotoxic compounds can also be generated by establishing anaerobic conditions and reducing the propitiousness of soil conditions to the pathogen or by means of different salts and toxins (Hoitink et al., 1991; Hoitink et al., 1997). The use of composts has also proved to decrease the population of several soil-borne pathogens including Fusarium spp. and R. solani (Bonanomi et al., 2020; Escuadra and Amemiya, 2008) and improved soil fertility based on the type of organic material used (Kallah and Adamu, 1998). Bonanomi et al. (2020) reported that pam compost, biochar, the fiber of coconut, sawdust, peat, and cellulose decreased Rhizoctonia populations.

The benefits of using organic soil amendments as soil additives are widely reported. However, the limited availability and the large quantities needed are the major challenges in the use of organic amendments for effective fungi control (Agrios, 2005).

Conclusion

This is a comprehensive review of the latest scientific knowledge and research works concerning mycotoxins and their phytotoxic impacts. It covers information on historical understanding and the production of various categories of mycotoxins and the respective fungal species responsible for the production of each phytotoxin. Reviews on the Rhizoctonia solani, which is responsible for the Rhizoctonia disease of potato, the anastomosis groups, and the epidemiology of Rhizoctonia solani. This review also contains information on the overview of phytotoxins, the various phytotoxins produced by Rhizoctonia solani, and the chemical structures. The Rhizoctonia solani is a known pathogenic fungus, which poses threat to the production of potatoes. The resulting losses associated with this fungus have been reported to be enormous. It is, therefore, important to make available, the various necessary information on research and knowledge about the fungus to help in the development of suitable measures to arrest the phytotoxic effects of the Rhizoctonia solani.

References

1. Abbas, A., Khan, S. U., Khan, W. U., Saleh, T. A., Khan, M. H. U., Ullah, S., Ali, A., Ikram, M. Antagonist effects of strains of Bacillus spp. Against Rhizoctonia solani for their protection against several plant diseases: Alternatives to chemical pesticides. Comptes Rendus Biologies, 2019, 342: 124–135.
2. Abdoulaye, A. H., Foda, M. F., Kotta-Loizou, I. Viruses Infecting the Plant Pathogenic Fungus Rhizoctonia solani. Viruses, 2019, 11: 1113.
3. Adesiyan, S. O., Caveness, F. E., Adeniji, M. O., Fawole, B. Nematode pests of tropical crops. Heinemann Educational Books Ltd, Ibadan, 1990, pp 19−26.
4. Ajayi-Oyetunde, O. O., Bradley, C. A. Rhizoctonia solani: taxonomy, population biology and management of Rhizoctonia seedling disease of soybean. Plant Pathology, 2018, 67: 3–17.
5. Alghisi, P., Favaron, F. Pectin degrading enzymes and plant-parasite interactions. European Journal of Plant Pathology, 1995, 101: 365−375.
6. Amadioha, A. C. Evaluation of some plant leaf extracts against Colletotrichum lindemuthianum in cowpea. Acta Phytopathologica et Entomologica Hungarica, 2003, 3(3−4): 259−265.
7. Anderson, N. A. The genetics and pathology of Rhizoctonia solani. Annual Review of Phytopathology, 1982, 20: 329−347.
8. Arici, S. E., Sanli, A. Effect of some essential oils against Rhizoctonia solani and Streptomycetes scabies on potato plants in field conditions. Annual Research and Review in Biology, 2014, 4(12): 2027−2036.
9. Aveskamp, M. M., De Gruyter, J., Crous, P. W. Biology and recent developments in the systematics of phoma, a complex genus of major quarantine significance. Fungal Divers, 2008, 31: 1−18.
10. Bagy, H. M. M. K., Hassan, E. A., Nafady, N. A., Dawood, M. F. A. Efficacy of arbuscular mycorrhizal fungi and endophytic strain Epicoccum nigrum ASU11 as biocontrol agents against blackleg disease of potato caused by bacterial strain Pectobacterium carotovora subsp. atrosepticum PHY7. Biological Control, 2019, 134: 103−113.
11. Bandy, B. P., Zanzinger, D. H., Tavantzis, S. M. Isolation of Anastomosis group 5 of Rhizoctonia disease from potato field soils in Maine. Phytopathology, 1984, 74: 1220−1224.
12. Bell, A. A., Wheeler, M. H., Liu, J, Stipanovic, R. D., Puckhaber, L. S, Orta, H. United States Department of Agriculture – Agricultural Research Service studies on polyketide toxins of Fusarium oxysporum f. sp. vasinfectum: potential targets for disease control. Pest Management Science, 2003, 59: 736−747.
13. Bennett, R. N., Wallsgrove, R. M. Secondary metabolites in plant defense mechanisms. New Phytologist, 1994, 127: 617−633.
14. Betancourt, O., Ciampi, L. Contribution to the study and control of Rhizoctonia solani. Isolation, extraction and bioassay of phenylacetic acid phytotoxicity produced in vitro by R. solani AG-3. Phytopathology, 2000, 35(2): 119−125.
15. Bonanomi, G., Zotti, M., Idbella, M, Di Silverio, N., Carrino, L., Cesarano, G., et al. Decomposition and organic amendments chemistry explain contrasting effects on plant growth promotion and suppression of Rhizoctonia solani damping off. PLoS ONE, 2020, 15(4): e0230925.
16. Bridge, J. Nematode management is sustainable and subsistence agriculture. Annual Review of Phytopathology, 1996, pp. 201−225.
17. Buiatti, M. Ingram, D. S. Phytotoxins as tools in breeding and selection of disease-resistant plants. Experientia, 1991, 47: 811−819.
18. Carla, R. M., Anne, C. K., Jean, D. The role of potatoes and potato components in cardiometabolic health: A review. Annals of Medicine, 2013, 45(7): 467−473.
19. Carling, D. E. Grouping in Rhizoctonia solani by hyphal anastomosis reaction. In: Sneh B, Jabaji-Hare S, Neate S, Dijst G, eds. Rhizoctonia species. Taxonomy, Molecular Biology, Ecology, Pathology and Disease Control, Kluwer Academic, Dordrecht, Netherlands, 1996, 37−47.
20. Carling, D. E., Kebler, K. M., Leiner, R. H. Interactions between Rhizoctonia solani AG-3 and 27 plant species. Plant Disease, 1986, 70(6): 577−578.
21. Chen, Y., Badillo-Vargas, I. E., Martin, K., Rotenberg, D., Whitfield, A. E. Characterization of novel thrips vector proteins that bind to tomato spotted wilt virus. (Abstr.) Phytopathology, 2019, 109: S2.1.
22. Coca Morante, M. “Potato Rhizoctonia Disease in the Bolivian High Andes”. EC Agriculture ,2019, 5.1: 15−23.
23. Cohen, Y., Baider, A., Cohen, B. H. Dimethomorph activity against oomycete fungal plant pathogens. Phytopathology, 1995, 85: 1500−1506.
24. Cook, D. E. L., Jenkins, P. D., Lewis, D. M. Production of phytotoxic spore germination liquids by Alternaria brassicae and Alternaria brassicicola and their effect on species of the family Brassicaceae. Annals of Applied Biology, 1997, 131: 413−426.
25. Craft, C. M., Nelson, E. B. Microbial properties of composts that suppress damping-off and root rot of creeping bentgrass caused by Pythium graminicola. Applied and Environmental Microbiology, 1996, 62: 1550−1557.
26. Date, H., Yagi, S., Okamoto, Y., Oniki, N. On the leaf blight of tomatoes by Thanatephorus cucumeris (Frank) Donk (Rhizoctonia solani). Annals of the Phytopathological Society of Japan, 1984, 50:399.
27. Diallo, S., Crepin, A., Barbey, C., Orange, N., Burini, J. F., Latour, X. Mechanisms and recent advances in biological control mediated through the potato rhizosphere. FEMS Microbiology Ecology, 2011, 75(3): 351−364.
28. Ding, L., Qin, S., Li, F., Chi, X., Laatsch, H. Isolation, antimicrobial activity, and metabolites of fungus Cladosporium sp. associated with red alga Porphyra yezoensis. Current Microbiology, 2008, 56: 229−235.
29. Dong, X., Ling, N., Wang, M., Shen, Q., Guo, S. Fusaric acid is a crucial factor in the disturbance of leaf water imbalance in Fusarium-infected banana plants. Plant Physiology and Biochemistry, 2012, 60: 171−179.
30. Escuadra, G. M. E., Amemiya, Y. Suppression of Fusarium wilt of spinach with compost amendments. Journal of General Plant Pathology, 2008, 74: 267−274.
31. Esfahani, M. N. Genetic variability and virulence of some Iranian Rhizoctonia solani isolates associated with stem canker and black scurf of potato (Solanum tuberosum L.). Journal of Plant Protection Research, 2020, 60 (1): 21–30.
32. Fernandes, G., Velangi, A, Wolever, T. M. S. Glycemic index of potatoes commonly consumed in North America. Journal of the American Dietetic Association, 2005, 105(4): 557−62.
33. Fewell, A. M., Roddick, J. G. Potato glycoalkaloid impairment of fungal development. Mycological Research, 1997, 101: 597−603.
34. Friedman, M. Potato glycoalkaloids and metabolites: Roles in the plant and in the diet. Journal of Agricultural and Food Chemistry, 2006, 54: 8655−8681.
35. Gibson, S., Kurilich, A. C. The nutritional value of potatoes and potato products in the UK diet. Nutrition Bulletin, 2013, 38(4): 389−399.
36. Gondal, A. S., Rauf, A., Naz, F. Anastomosis Groups of Rhizoctonia solani associated with tomato foot rot in Pothohar Region of Pakistan. Scientific Reports, 2019, 9: 3910.
37. Gouda, S., Kerry, R. G., Das, G., Paramithiotis, S., Shin, H. S., Patra, J. K. Revitalization of plant growth promoting rhizobacteria for sustainable development in agriculture. Microbiological Research, 2018, 206: 131−140.
38. Grainge, M., Almed, S. Handbook of Plants with Pest – Control Properties. John Wiley and Sons, New York, 1988.
39. Gururani, M. A., Upadhyaya, C. P., Baskar, V., Venkatesh, J., Nookaraju, A., Park, S. W. Plant growth-promoting rhizobacteria enhance abiotic stress tolerance in Solanum tuberosum through inducing changes in the expression of ROS-scavenging enzymes and improved photosynthetic performance. Journal of Plant Growth Regulation, 2013, 32: 245−258.
40. Hartill, W. F. T. Some effects of Rhizoctonia solani on growth and yield of potatoes. Potato Research, 1989, 32(3): 283−292.
41. Herrmann, K. M., Weaver, L. M. The shikimate pathway. Annual Review of Plant Physiology, 1999, 50: 473−503.
42. Hoitink, H. A. J., Boehm, M. J. Biocontrol within the context of soil microbial communities: A substrate-dependent phenomenon. Annual Review of Phytopathology, 1999, 37: 427−446.
43. Hoitink, H. A. J., Inbar, Y., Boehm, M. J. Status of compost-amended potting mixes naturally suppressive to soil-borne diseases of horticultural crops. Plant Disease, 1991, 75: 869−873.
44. Hoitink, H. A. J., Stone, A. G., Han, D. Y. Suppression of plant disease by composts. Horticultural Science, 1997, 32: 184−187.
45. Hu, W., Pan, X., Li, F., Dong, W. UPLC-QTOF-MS metabolomics analysis revealed the contributions of metabolites to the pathogenesis of Rhizoctonia solani strain AG-1-IA. PLoS One, 2018, 13(2): e0192486.
46. Ibraheem, S. A., Okesha, A. M., Mihathem, K. T. Interrelationship between protein and oil content of soybean seed with some associated fungi. Journal of Agricultural, Water Resources and Research in Plant Production, 1987, 6: 53−66.
47. Isakeit, T. 2011. Rhizoctonia canker and black scurf of potato. Texas AgriLife Extension, PLPA-POT003−2011.
48. Ito, M., Meguro-Maoka, A., Maoka, T., Akino, S., Masuta, C. Increased susceptibility of potato to Rhizoctonia diseases in potato leaf roll virus-infected plants. Journal of General Plant Pathology, 2017, 83: 169–172.
49. Jiang, H., Qi, P., Wang, T., Chi, X., Wang, M., Chen, M., Chen, N., Pan, L. Role of halotolerant phosphate-solubilizing bacteria on growth promotion of peanut (Arachis hypogaea) under saline soil. Annals of Applied Biology, 2019, 174: 2–30.
50. [bookmark: _Hlk52695829]Johnson, S. B., Leach, S.S. Bulletin #2273, Potato Facts: Rhizoctonia Diseases on Potatoes. The University of Maine Cooperative. Extension, 2020, 2–7.
51. Johnson, D. A., Cummings, T. F., Hamm, P. B. Cost of fungicides used to manage potato late blight in the Columbia Basin: 1996 to 1998. Plant Disease, 2000, 84: 399−402.
52. Kallah, P., Adamu, R. Annual manure intensive vegetable garden for profit and self-sufficiency. Peace Crop information collection and Exchange, 1998, pp. 5−8.
53. Kankam, F., Long, H., He, J., Zhang C., Zhang, H., Pu, L. and Qiu, H. 3-Methylthiopropionic acid of Rhizoctonia solani AG-3 and its role in the pathogenicity of the fungus. The Plant Pathology Journal, 2016b, 32(2): 85−94.
54. Kankam, F., Pu, Qiu, H., Pu, L., Long, H., He, J., Zhang, C, and Zhang, H. Isolation, purification and characterization of phytotoxins produced by Rhizoctonia solani AG-3, the cause agent of potato stem canker. American Journal of Potato Research, 2016a, 93(4): 321−330.
55. Kankam, F., Sowley, E. N. K. and Abdulai, I. Evaluation of cowpea (Vigna unguiculata) genotypes for resistance to web blight caused by Rhizoctonia solani. Asian Journal of Research in Crop Science, 2018, 2(3): 1−7.
56. Kankam, F., Sowley, E. N. K., Qiu, H. Influence of 3-Methylthiopropionic Acid (MTPA) Produced by Rhizoctonia solani AG-3 on Yield and Dry Matter Accumulation of Potato. Asian Journal of Research in Crop Science, 2018, 2(2): 1-9.
57. Kara, A., Arici, S. E. Determination of Gamma Rays Efficiency against Rhizoctonia solani in Potatoes. Open Chem., 2019, 17: 254–259.
58. Karban, R. The ecology and evolution of induced resistance against herbivores. Functional Ecology, 2011; 25:339−347.
59. Katan, J. Cultural approaches for disease management: present status and future prospects. Journal of Plant Pathology, 2010, 92(4 Supplement): S4.7−S4.9.
60. Kataria, H. R., Hugelshofer, D., Gisi, D. Sensitivity of Rhizoctonia species to different fungicides. Plant Pathology, 1991, 40: 203−211. .
61. Kouzai, Y., Kimura, M., Watanabe, M., Kusunoki, K., Osaka, D., Suzuki, T., Matsui, H., Yamamoto, M., Ichinose, Y., Toyoda, K. Salicylic acid-dependent immunity contributes to resistance against Rhizoctonia solani, a necrotrophic fungal agent of sheath blight, in rice and Brachypodium distachyon. New Phytologist, 2018, 217: 771–783.
62. Lai, M., Weinhold, A. R., Hancook, J. G. Permeability changes in Phaseolus aureus associated with infection by Rhizoctonia solani. Phytopathology, 1968, 58: 240−245.
63. Lakshman, D. K., Liu, C. Y., Mishra, P. K., Tavantzis, S. Characterization of the arom gene in Rhizoctonia solani and transcription patterns under stable and induced hypovirulence conditions. Current Genetics, 2006, 49: 166−177.
64. Larkin, R. P., Griffin, T. S., Honeycutt, C. W. Rotation and cover crop effects on soil-borne potato diseases, tuber yield, and soil microbial communities. Plant Disease, 2010, 94: 1491−1502.
65. Larkin, R. P., Brewer, M. T. Effects of crop rotation and biocontrol amendments on Rhizoctonia disease of potato and soil microbial communities. Agriculture, 2020, 10: 128.
66. Liang, L., Zheng, A. Preliminary characterization of the phytotoxin of sheath-blight disease of rice caused by Rhizoctonia solani. African Journal of Biotechnology, 2012, 11(29): 7520−7527.
67. Liu, C. Y, Lakshman, D. K, Tavantzis, S. M. Quinic acid induces hypovirulence and expression of a hypovirulence-associated double-stranded RNA in Rhizoctonia solani. Current Genetics, 2003b, 43: 103−111.
68. Liu, C., Lakshman, D. K., Tavantzis, S. M. Expression of a hypovirulence-causing double stranded RNA is associated with up-regulation of quinic acid pathway and down regulation of shikimic acid pathway in Rhizoctonia solani. Current Genetics, 2003a, 42: 284−291.
69. Madhavi, G. B., Devi, G. U., Kumar, K. V. K., Ramesh, T. Evaluation of Pseudomonas fluorescens and Trichoderma harzianum isolates in inducing systemic resistance (ISR) in maize against Rhizoctonia solani f. sp Sasakii. International Journal of Consumer Studies, 2018, 6(2): 628–632.
70. Mekonnen, H., Fenta, L. Plant Growth Promoting Rhizobacteria for Plant Growth Promotion and Biocontrol Agent against Tomato and Pepper Disease: A review. World News of Natural Sciences, 2020, 28: 132–3.
71. Morrissey, J. P., Osbourn, A. E. Fungal resistance to plant antibiotics as a mechanism of pathogenesis. Microbiology and Molecular Biology Reviews, 1999, 63: 708−724.
72. Murray, D. I. L. Penetration of barley root and coleoptile surfaces by Rhizoctonia solani. Transactions of the British Mycological Society, 1982, 79: 354−360.
73. Muzhinji, N., Truter, M., van der Waals, J. E. First report of Rhizoctonia solani AG 4HG-III causing potato stem canker in South Africa. Plant Disease, 2015, 100: 555–564.