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Review

Sheath Blight of Maize: An Overview and Prospects for Future Research Directions

by
Runze Di
1,2,†,
Lun Liu
1,2,†,
Noman Shoaib
3,4,
Boai Xi
1,
Qiyan Zhou
1 and
Guowu Yu
1,2,*
1
State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu 611130, China
2
National Demonstration Center for Experimental Crop Science Education, College of Agronomy, Sichuan Agricultural University, Chengdu 611130, China
3
CAS Key Laboratory of Mountain Ecological Restoration and Bioresource Utilization & Ecological Restoration Biodiversity Conservation Key Laboratory of Sichuan Province, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610041, China
4
University of Chinese Academy of Sciences, Beijing 101408, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Agriculture 2023, 13(10), 2006; https://doi.org/10.3390/agriculture13102006
Submission received: 5 September 2023 / Revised: 28 September 2023 / Accepted: 5 October 2023 / Published: 16 October 2023
(This article belongs to the Special Issue Advances in Biological Control of Plant Diseases)
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Abstract

:
Sheath blight (ShB) of maize, as a soil-borne disease caused by Rhizoctonia solani AG1-IA, is one of the main obstacles for maintaining the sustainable production of maize. R. solani has a wide host range and low-resistance sources, there is a lack of resistant resources against ShB, and the damage caused by ShB cannot be effectively controlled. To effectively protect crops against ShB, it is necessary to combine information about its pathogenicity and about the disease prevention and control of the pathogenic fungus and to identify areas that require more in-depth research. While progress has been made in the identification of disease-related genes in corn and pathogens, their mechanisms remain unclear. Research related to disease control involves the use of agronomic methods, chemical control, biological control, and genetic improvement. Breeding and identification of high-resistant maize varieties are key and difficult points in the control of maize sheath blight. This article reviews the research progress of the symptoms, the pathogen’s biological characteristics, the infection process, the pathogenic mechanism, and comprehensive control of maize sheath blight disease and provides future research directions of maize sheath blight in China. It aims to provide reliable technical routes and research ideas for future crop-disease-resistance research, especially to sheath blight of maize.

1. Introduction

Maize is China’s main food source, feed crop, and industrial raw material and plays an important role in the national economy and agricultural production. However, biological and abiotic stresses have always been an important factor limiting a high and stable yield of maize [1,2]. In recent years, due to the occurrence of various diseases, the maize-producing areas have been seriously damaged by diseases, resulting in the loss of maize yield and a deterioration in its quality. ShB is one of the most widespread and serious diseases in maize when it was planted in humid weather areas [3]. The earliest records of the occurrence of maize sheath blight in China were found in Jilin Province [4,5]. We summarize the research history of sheath blight and list its important research progress (Table 1) [4,5,6,7,8,9,10,11,12].
In recent years, the expansion of the field of planting, the promotion of high-yield and dense-planting technology, and the increase in fertilization have caused the occurrence, development, and spread of maize sheath blight. And, the resultant damage is becoming more and more serious. The general incidence rate is 70–100%, the resultant yield loss is 10–20%, and the yield loss can be as high as 35%. Maize sheath blight has become one of the main diseases in maize-producing areas in China [13,14,15,16,17]. Although some pathogenic-related genes have been cloned and their functions have been verified, their regulatory network is not very clear (Table 2) [12,18,19,20,21,22]. Using these genes to carry out breeding for sheath blight resistance still has a long way to go. Therefore, the prevention and control of maize sheath blight in China are still facing severe challenges [23,24].

2. Symptoms of Maize Sheath Blight Infection

Maize sheath blight can occur at any stage of maize growth, from the seedling to the late growth. It mainly affects the leaf sheaths, leaves, bracts, and stems of maize, potentially causing severe ear damage. The pathogen initially infects 1–2 stem nodes and leaf sheaths near the ground, gradually spreading upwards. The lesions initially appear water-soaked and often take on an irregular or elliptical shape. As the disease advances, these lesions can expand, merging to create irregular, moiré-like patterns, ultimately leading to the withering of leaf sheaths and leaves. This same moiré-like pattern can develop on the ear, resulting in ear rot, which can be highly detrimental (Figure 1). When the air humidity and the temperature are high, the disease exhibits dense white mycelium growth. Over time, the mycelium gradually changes color and forms a sclerotic of different sizes. Crucially, the hyphae within these sclerotia can survive through the winter and serve as the primary infection source in the following year [25,26].

3. Sheath Blight Pathogen Biology

3.1. Biological Characteristics

The pathogens causing maize sheath blight are three soil-dwelling fungi including Rhizoctonia solani, Rhizoctonia zeae, and Rhizoctonia cerealis [25]. Due to the variations in sample sources and locations, there are differences in the composition of maize sheath blight pathogen species [27]. The primary pathogen causing maize sheath blight in China is R. solani. This fungus was first observed on diseased potato tubers by Julius Kuhn in 1858 and named R. solani [28]. It exhibits a wide host range, capable of infecting 263 plant species in 43 families [10,29]. Based on the analysis of its compatibility with the hyphal fusions of the known test strains, it has been categorized into different anastomotic groups (AGs). Over time, the number of AGs has increased from the initial 6 to 14 (AG-1 to AG-13 and AG-BI), showing significant variability in colony morphology, host range, aggressiveness, and nutrient requirements [30,31,32,33]. Based on the sequence homology, size, and shape of the sclerotium, AG1 strains are further divided into three subgroups, IA, IB, and IC, all of which can cause sheath blight, with AG1-IA being the dominant pathogen [34,35,36].
The AG1-IA colonies exhibit rapid growth, forming white colonies on a potato medium (PDA) at 28 °C. Typically, the entire dish becomes covered in 2 days of cultivation. These colonies display the distinctive separation and constriction features characteristic of Rhizoctonia. After 2–3 days, sclerotia developed around the petri dish, eventually turning brown with a rough surface and varying in size (Figure 2).
The growth temperature of the strain ranges from 7 to 39 °C, with an optimum temperature between 26 and 30 °C. Sclerotia formation occurs between 11 and 37 °C, with optimum conditions at 22 °C and a suitable pH range of 5.4 to 7.3 [37,38]. Sunlight stimulates strain formation, and sclerotia are notably resistant to ultraviolet light. In conditions of high temperature and humidity, the fungus grows rapidly. Sclerotia germinate and produce hyphae in 1–2 days and then produce new sclerotia in 6–10 days. Initially, sclerotia are white but gradually turn brown upon maturity due to the formation of melanin in the cell wall. This melanin has the hydrophobic properties of oxidized phenols, which reduce cell wall permeability and protect cells from biodegradation. Sclerotia are rich in protein, polyphosphates, glycogen, and lipid nutrients in the cytoplasm. These can be used as energy sources under extreme environmental conditions and support the re-infection process. Typically, sclerotia remain dormant, but if they encounter a suitable environment, they can break this dormancy and re-germinate into pathogenic hyphae [39].

3.2. Pathogen Infection and Disease Cycle

Maize sheath blight is caused by Rhizoctonia solani. Symptoms of sheath blight can be observed on all aerial parts of the maize plant except the tassel. The fungus can survive as sclerotia or mycelium in the remains of host plants [40,41]. Due to favorable humidity and temperature, sclerotia in the soil germinate, growing hyphae that infect the basal leaf sheaths of the maize plant. These hyphae grow on the maize leaf sheaths, forming infestation mats. The pathogens then colonize the entire plant via surface hyphae, creating new infection areas with characteristic symptoms [42]. Eventually, the lesions on the upper parts of the leaves fuse, covering the entire stem and sheath of the plant. This leads to stem lodging, disrupts water transport, interferes with the canopy structure, reduces photosynthetic capacity, and can ultimately cause the plants to die.
After the maize is harvested, R. solani from infected plants survives as sclerotia or mycelium in the soil and on infected crop residues for extended periods, becoming a source of infection for subsequent crop cycles. The fungus spreads through water, contaminated soil, and plant debris. Its growth is attracted to newly planted host crops, and it infects plants due to chemical irritants released by growing plant cells [43,44]. It is found that maize sheath blight can invade the host through the epidermis, stomata, and natural orifices [45]. The primary mode of invasion is through the epidermis, and it gradually spreads upwards, affecting stems, sheaths, leaves, and ears. During rainy and humid conditions, the lesions produce white mycelium, and the spores are dispersed with the wind, leading to re-infection. Overwintering fungi exist in the form of sclerotia or infected crop residues (Figure 3).
For some R. solani diseases, the formation of the infection structure is related to the pathogenicity of the pathogen and the resistance of the host. When the pathogenic fungus exhibits strong pathogenicity or the host has poor resistance, the fungus infects rapidly, the mycelium spreads quickly, and it readily forms numerous infection structures. Conversely, when the infection rate is slow, only a few infection structures may form. Basu was the first to report the ultrastructural differences between resistant and susceptible varieties of R. solani [46]. The study found that, compared to resistant varieties, pathogens tend to grow more hyphae on susceptible varieties, exhibit more branching, and maintain closer contact with the host. They can form a greater number of intercellular and intracellular structures and are more prone to producing a large quantity of sclerotia. The infection process of the pathogen on Zoysia japonica primarily comprises four stages: adsorption, directional growth, infiltration, and colonization. The hyphae form an infection pad on the plant surface, and then invade the plant tissue through the intercellular space. Mycelial infection does not directly result in lesion formation [47].

3.3. Pathogenic Mechanism of Pathogenic Fungus

During their long-term evolution and intricate interactions with plants, pathogenic fungi have developed parasitism and pathogenicity towards plants. Phytopathogenic fungi produce metabolites harmful to parasitic plants, termed pathogenic factors. These primarily fall into three categories: enzymes, toxins, and hormones [32,33,34]. With the publication of the whole genome sequence of R. solani AG1-1A and the maize genome sequence, valuable resources are now available to uncover the key mechanisms of sheath blight infection and disease [48,49]. Research has shown that sheath blight primarily produces three types of cell-wall-degrading enzymes and toxins: polygalacturonase (PG), polymethylgalacturonase (PMG), and cellulase (Cx). These cell-wall-degrading enzymes and toxins have a pronounced leaching effect on leaves and leaf sheaths. During infection with R. solani, the host plants are damaged with the secretion of enzymes and small toxins [50]. Furthermore, R. solani was found to produce the RS toxin, a mixture of glucose, mannose, N-acetylgalactosamine, and N-acetylglucosamine. Strains isolated from tomato and cotton produce toxins similar to this, which can induce characteristic symptoms in plants [51]. Sriram et al. isolated a toxin produced using R. solani, and an analysis showed that this toxin was primarily composed of glucose and mannose [52]. It was discovered that after infecting the host, the pathogen can produce certain virulence factors that inhibit the synthesis of chlorophyll and the absorption of CO2 in the host tissue, leading to a decrease in photosynthesis [53]. When maize is infected with R. solani, differentially expressed genes are involved in signal transduction, cellular material transport, protein synthesis and transport, secondary metabolism, and more [14]. A transcriptome analysis of maize infected with R. solani revealed that multiple genes, such as extracellular proteases, ABC transporters, and transcription factors, play roles in the establishment of infection. During the nutrient deprivation phase of infection, there are changes in the expression of genes associated with sugar transporters, cellular metabolism, and protein degradation [54].
When plants are invaded by pathogens such as R. solani, they activate two distinct immune responses (Figure 4). The first layer is pathogen-associated molecular pattern-triggered immunity (PTI). PTI primarily induces the release of reactive oxygen species (ROS) by sensing the pathogen-associated molecular pattern through membrane-associated pattern recognition receptors (PRRs). This process involves the entry of calcium ions (Ca2+) through the plasma membrane and the activation cascade of calcium-dependent kinases (CPK), CBL-interacting protein kinases (CIPK), G proteins, and mitogen-activated protein kinases (MAPK), thereby activating the defense signaling cascade in plant cells. The second layer is effector-triggered immunity (ETI). ETI is initiated with the recognition of pathogen-related effectors using intracellular nucleotide-bound leucine-rich repeat receptors (NLRs), leading to strong immune responses, such as the hypersensitive response (HR). Pruitt et al. found that these two layers have a synergistic immune effect and together regulate the plant’s immune response [55]. Recent studies have indicated that PTI is involved in resistance to Rhizoctonia solani in maize. For instance, ZmGABA-T inhibits allergic necrosis induced with EG1 through its interaction with EG1, conferring resistance to R. solani infection. Whether ETI is involved remains unclear.
The signal transduction mechanism of R. solani infection remains unclear but might involve G-protein-mediated signaling through second messengers, including cAMP (cyclic adenosine monophosphate) and numerous downstream pathogenic effector molecules. G proteins represent the largest group of cell wall receptors in fungi and play crucial roles in promoting survival, reproduction, and virulence. Disruption of the G protein leads to slow fungal growth, diminished pathogenicity, alterations in colony structure, and an inability to form sclerotia. For other pathogenic fungi, changes in cAMP levels have been reported following G protein disruption during infection, which affects downstream effector molecules involved in enhancing plant infection or suppressing plant defense responses. The effector molecules identified in different R. solani strains have shown significant diversity in gene sequences, indicating adaptation and flexibility (through gene duplications, deletions, and point mutations) to evade host recognition and optimize virulence function. This adaptability might be one of the potential factors contributing to the broad host range of R. solani strains [56,57,58,59].

3.4. Study on the Resistance Mechanism of Maize Sheath Blight

When plants are infected with non-compatible pathogens, there are primarily two levels of defense systems. The first is the structural and chemical factors of the plant itself, which include cell wall cutin, wax, lignin, chitinase, glycanases, phytochemicals, and toxic phenolic compounds. The second defense system, induced by pathogens, encompasses the hypersensitive reaction (HR) and systemic acquired resistance [60]. Tang discovered that the disease resistance of maize is closely associated with certain sugars (like sucrose and soluble sugar) and proteins (such as soluble protein and free amino acid content) [61]. Liu determined the resistance of maize materials by measuring the variations in peroxidase, catalase, and superoxide dismutase in the leaves of maize sheath-blight-resistant material R15 and susceptible material Ye478 after inoculation [62]. Pathogenicity is positively correlated with the levels of hydrogen peroxide and peroxidase in maize. These defense enzymes may work in tandem in maize, enabling plants to counteract pathogen attacks. Deng observed that the resistance variations in maize sheath blight, both by variety and stage, were linked to the activity of phenylalanine ammonia lyase [63]. Sharma’s research indicated that after disease-resistant maize varieties were infected with R. solani, less MDA accumulated in the leaf sheath tissue, whereas more MDA was produced in susceptible varieties [64].
The resistance to sheath blight varied significantly among different maize lines and varieties, with most lines and varieties exhibiting weak resistance to sheath blight. Zhang identified 65 maize materials from various sources and genetic types for resistance to sheath blight under artificial inoculation conditions [65]. No immune or highly resistant materials were found. The resistant and moderately resistant materials accounted for 3.1% and 13.9%, respectively. Yang [66] conducted field disease resistance tests on 45 maize inbred lines collected from across the country. He found no inbred lines that were immune to sheath blight. Highly resistant materials made up 2.2% of the total identified, 17.8% were moderately resistant, 55.6% were moderately sensitive, and 24.4% were highly sensitive. Notably, Mo17, Huangzaosi, and Y478, which are extensively used in China’s maize production, are outstanding inbred lines with moderately high resistance to maize sheath blight. Over many years, Yang employed the multi-point manual inoculation identification method to assess 203 maize resource materials [67]. Among the identified materials, CML270 stood out as a resistant material with both high and stable resistance.

4. Prevention and Treatment of Maize Sheath Blight

4.1. Selection of Resistant Germplasm Resources

Banded leaf and sheath blight (BLSB) is a major disease, most prevalent in tropical regions of the world, especially in south and southeast Asian countries, and specifically in India during the Kharif season [23]. In recent years, national programs in India, China, Indonesia, and the Philippines have worked to screen for BLSB-resistant genotypes. Under the All India Coordinated Research Project (AICRP) on maize, the response of inbred and hybrid strains to BLSB has been evaluated, and several strains with moderate resistance levels have been identified [15]. Xie et al. proposed a patented technique for breeding resistant strains of maize sheath wilt [68]. The combining ability was determined using the Guangxi backbone line and the American backbone line. Materials with high resistance to maize sheath wilt, and those with high resistance heritability, excellent comprehensive traits, and high general combining ability, were chosen as the primary resistant transfer parents. The S1 generation was obtained from spring N + 1 using bagging. This S1 generation was then planted in autumn N + 1 and artificially inoculated with sheath wilt. Plants with desirable comprehensive traits, such as synchronized male and female flowering, disease resistance, and fallback resistance, were selected for self-crossing. Poor-performing seed rows were eliminated during seeding, with the remainder progressing to the S2 generation. Subsequent self-crossing was conducted from the S3–S10 generations for planting identification and screening, along with artificial inoculation for grain wilt. Single plant selection was based on target traits like good grain quality, fruitful yield, and disease resistance. Several genotypic homozygous and phenotypic inbred lines were developed with the S10 generation. Ultimately, 247 new breeding materials with high resistance to maize sheath blight, suitable for Guangxi, were successfully selected.

4.2. Agronomic Measures

Sclerotia left in the field for overwintering are a significant source of the disease’s initial infection. Regular monitoring of the inoculum and removal of weed hosts play a crucial role in sheath blight management. Peeling off susceptible leaf sheaths and leaves can cut off the re-infection source of sheath blight, preventing the disease from further expanding and spreading. It is essential to choose relatively resistant varieties and sow them in a timely and appropriate quantity. Optimizing the use of nitrogen fertilizers can boost yield while preventing disease spread and fungal infection. Maintaining optimal plant density and using the right concentration of fungicides, along with removing host weeds at the field boundary, are also vital. Strengthening field management and reducing the rotation of host plants can help mitigate the impact of maize sheath blight [69,70,71,72].

4.3. Chemical Control

The most common method for controlling sheath blight is the use of fungicides [73,74,75,76]. Biocides are toxic substances, typically compounds (either natural or synthetic), that have a unique mode of action. They can kill fungi through various means, such as disrupting fungal cell membranes, acting as enzyme inhibitors, interfering with respiration or energy production processes, or inhibiting the formation of cell walls. The most effective chemical agents for controlling maize sheath blight include Jinggangmycin, trigonin, carbendazim, and thiophanate. Among these, Jinggangmycin has the most potent control effect [77,78]. Jinggangmycin exhibits varying control effects at different growth stages of maize and varying disease severities. Using fungicides at low levels is highly effective in controlling fungal diseases in crops. A series of 1,3,4-oxadiazole derivatives were synthesized from benzoylhydrazine and aromatic aldehydes through condensation and oxidative cyclization, demonstrating active antifungal activity [79]. However, it is important to note that prolonged use of a single fungicide can elevate the risk of fungi developing resistance to that specific fungicide. For instance, Rhizoctonia solani can develop multiple-drug resistance (MDR) through metabolomic and exodal activity [80]. Mutations in fungal genomes might lead to altered target sites for fungicide binding, increased production of target proteins, decreased fungicide uptake, or heightened metabolic degradation. As a result, the composition of fungicides is frequently adjusted to improve their specificity in identifying and targeting fungi [81,82,83].

4.4. Biological Control

Biological control involves the use of parasites, predators, or microorganisms (biocontrol agents) to decrease the population of pests or pathogens. It is generally viewed as a safe and effective method for managing plant diseases [84,85,86]. Plant-growth-promoting rhizobia (PGPR) are beneficial fungi in the rhizosphere. They play a role in the biosynthesis of plant hormones such as indoleacetic acid, gibberellin, and abscisic acid, enhance nitrogen uptake, facilitate phosphate solubilization, and interfere with pathogen toxin production [87]. Pseudomonas fluorescens combats R. solani by producing antimicrobial compounds like hydrogen cyanide, β-1,3 glucanase, and chitinase, which can be applied as foliar sprays or soil amendments [88]. Pseudomonas aeruginosa is among the most researched and successful plant symbionts within fungi that promote rhizosphere growth and endophytes. It can directly antagonize pathogens or trigger systemic resistance, offering protection against a broader range of plant pathogens [89,90]. The Pseudomonas aeruginosa strain MF-30, isolated from the maize rhizosphere, possesses plant-growth-promoting properties. Foliar spraying with this strain can notably boost antioxidant defense enzymes in plants while decreasing H2O2 concentration. It can also significantly reduce disease severity and lesion length, and enhance the accumulation of biomass in the roots and stems of maize plants pre-inoculated with sheath blight. This makes it a potential biological control agent for resisting pathogen infection under pathogenic stress [87]. Eukaryotic microorganisms, specifically fungi like Trichoderma, have been employed as antagonists for R. solani control. They inhibit R. solani by competing for nutrients and through fungal parasitism, which involves the production of antifungal secondary metabolites. When applied as a foliar spray, a reduction in the occurrence of maize sheath blight was observed [91]. It was discovered that the parasitic Trichoderma viride (Tviride), which is parasitic on Gastrodia-dependent Cyclocystis, exhibited an antagonistic effect on maize sheath blight, with a control rate of 74% and hyperparasitism [37]. Chen Jie and colleagues tested two biological pesticides produced in the United States, BG (Botani Gard) and Soigard, as well as a domestically produced biological seed coating (ZSB) on maize during both the seedling and adult stages. In the sheath blight control experiment with BG-2, it was found that BG-2 had a notable control effect on the occurrence of maize sheath blight [44] (Figure 5). A new bacterial strain, Bacillus halotolerans LDFZ001, demonstrated efficient antagonistic activity against the pathogenic strain Rhizoctonia solani [92]. The Bacillus polymyxoides SF05 strain can also be utilized to control maize sheath wilt and induce systemic resistance [93]. In Mexico, a formulation and mesoporous material of Beauveria bassiana MABb1 were employed for the biological control of maize sheath wilt [94].

4.5. Genetic Improvement in Maize Sheath Blight Resistance

The resistance of maize to sheath blight is a quantitative trait controlled with multiple genes. QTL (quantitative trait locus) mapping reveals the association between genes, loci, and traits, which has been utilized for marker-assisted selection in breeding [8,95,96]. Quantitative trait loci related to resistance have been identified on all 10 pairs of maize chromosomes (Table 3), with a high distribution frequency on chromosomes 1, 2, 4, and 6 [15,66,97,98,99,100,101,102,103,104,105]. Wisser summarized 437 dQTLs and 17 major disease resistance genes from 50 studies on the genetic structure of maize disease resistance [106]. The results indicated that QTLs were distributed in a somewhat non-random manner across the genome. An analysis of multiple maize inbred lines revealed strong genetic correlations between resistance to three foliar diseases in a population of 253 different lines, suggesting that some genes confer multiple resistances [107]. A recent Genome-Wide Association Study (GWAS) identified 28 SNP loci significantly associated with sheath blight resistance, based on 318 inbred lines. For the first time, several maize sheath blight resistance genes were cloned. One such resistance gene, ZmFBL41, confers sheath blight resistance through a natural mutation that prevents the inhibition of lignin synthesis with the pathogenic fungus [105]. This research offers a crucial theoretical foundation and genetic resources for enhancing the resistance of maize and other crops to sheath blight, holding significant value for the genetic improvement in crop resistance to this disease.
The use of gene modification and gene editing technologies in plant biotechnology has broadened the potential for targeted gene suppression to curb pathogenicity. Upon sensing a pathogen attack, plant defense mechanisms are activated. These mechanisms include hypersensitivity responses, production of reactive oxygen species (ROS), accumulation of secondary metabolites (such as phytoalexins, phenols, and tannins), and the production and accumulation of pathogenesis-related (PR) proteins [108]. Currently, there are limited reports on resistance genes that can effectively control maize sheath blight both domestically and internationally. However, numerous studies have confirmed that introducing certain broad-spectrum disease resistance genes into crops like rice and wheat through genetic engineering can significantly enhance resistance to sheath blight. These studies provide valuable insights for developing sheath-blight-resistant maize varieties. Rice plants that overexpress the PR gene (Oryza sativa Chitinase 11) inhibit R. oryzae by hydrolyzing the β-1,4 glycosidic bonds of N-acetylglucosamine polymers in fungal chitin, thereby degrading the fungal cell wall [109]. Liu introduced the cloned wheat-derived pathogen-inducible gene TaPIEP1 into Yang wheat. It was found that the TaPIEP1 gene was overexpressed in the resulting wheat transformants and could be passed on to their progeny [110]. Some of these wheat transformants, which exhibited high exogenous DNA expression efficiency, displayed notable resistance to both wheat scab and wheat sheath blight.
CRISPR/Cas9 editing technology has been employed to inhibit the growth of Rhizoctonia solani in rice. R. solani activates the OsSWEET11 sugar transporter in infected plant cells to expel sugar molecules for its nourishment. Pathogen infection experiments revealed that OsSWEET11-knockout mutants, created using CRISPR-Cas9 technology, were less susceptible to ShB compared to wild-type plants that overexpressed OsSWEET11. By controlling the expression of OsSWEET11, plants can be shielded from infection without compromising crop yield [111]. Plants overexpressing ZmFBL41 exhibited increased susceptibility to R. solani [11]. The OsGABA-T-knockout plants displayed heightened susceptibility to R. solani, manifesting larger lesions [22]. ZmNAC41 transgenic materials demonstrated resistance to sheath blight [12]. The precision of gene editing technology, especially for creating loss-of-function mutations, makes it a promising tool for crop improvement.

5. Prospects

Maize sheath blight is a soil-borne disease. R. solani, the causative agent of sheath blight, has a broad host range, is harmful, and lacks a singular disease resistance gene. Current research primarily addresses the occurrence, spread, and control of sheath blight. The breeding and identification of highly resistant maize varieties are pivotal and challenging aspects of controlling maize sheath blight. The most prevalent method remains the use of fungicides. However, their prolonged use can result in accumulation in agricultural soils and groundwater contamination, adversely affecting the environment and leading to pathogen resistance over time. Thus, managing sheath blight in maize necessitates a reduced dependence on synthetic fungicides in favor of natural fungicides and biological agents. In this context, nanotechnology offers potential solutions for maize sheath blight control. For instance, essential-oil-grafted copper nanoparticles could serve as a potential next-generation fungicide for comprehensive disease management in maize [112]. Additionally, nanosheet-facilitated dsRNA spray delivery presents a promising tool for controlling Sclerotinia rickura infection [113].
Additionally, exploring combinations of natural fungicides, biologics, and antibiotics to combat sheath blight infection with R. solani could be a more sustainable approach. Due to the rapid spread of sheath blight, when plants are closely spaced and nitrogen fertilizers are overused, it exacerbates the problem. Thus, adopting wider spacing and sparse planting to prevent plant-to-plant contact, along with management practices like post-harvest drying and field cleaning, can help prevent re-infection. While QTL analyses have pinpointed some potential ShB resistance loci, the underlying mechanisms of pathogenicity and resistance remain elusive and warrant further investigation. Although genes related to various stages of sheath blight pathogenesis have been identified, further validation of these genes will guide the development of ShB-tolerant varieties and assist in screening and selecting disease-resistant strains. Understanding the optimal conditions for R. solani infection will also aid in the screening and selection of superior disease-resistant varieties. Utilizing tolerant, and ideally resistant, varieties represents another sustainable strategy. Currently, there are no effective immune or highly resistant materials against sheath blight. Therefore, it is essential to leverage the identified and screened resistant materials, intensify research on the localization and cloning of maize sheath blight resistance genes, and employ biotechnological methods, such as transgenics, to expedite the breeding for sheath blight resistance.

Author Contributions

G.Y. and R.D. designed and wrote the review. L.L., N.S., B.X. and Q.Z. analyzed the whole article. G.Y. read and approved the contents. All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by the China Agriculture Research System (CARS05), Natural Science Foundation of China (Nos.: 31501322 and 31971960), Postdoctoral Special Foundation of Sichuan Province (No.: 03130104), and Overseas Scholar Science and Technology Activities Project Merit Funding (No.: 00124300).

Institutional Review Board Statement

Not applicable.

Data Availability Statement

Not applicable.

Acknowledgments

This work was partly supported by the Maize Research Institute, Sichuan Agricultural University.

Conflicts of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Figure 1. The sheath blight on maize with Rhizoctonia solani. (a): plant; (b): leaf; (c): stem; and (d): ear.
Figure 1. The sheath blight on maize with Rhizoctonia solani. (a): plant; (b): leaf; (c): stem; and (d): ear.
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Figure 2. The growth of Rhizoctonia solani on PDA.
Figure 2. The growth of Rhizoctonia solani on PDA.
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Figure 3. The disease cycle of sheath blight of maize.
Figure 3. The disease cycle of sheath blight of maize.
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Figure 4. Molecular mechanisms of maize response to Rhizoctonia solani infection. RBOH: respiratory burst oxidase homolog; CNGC: Ca2+ channel protein; POX: peroxidase; PAL: phenylalaninammo—nialyase; POD: peroxidase isozyme; SOD: superoxide dismutase; CAT: catalase; APX: ascorbate peroxidase; GPX: glutathione peroxidase; AOC: allene oxide cyclase; AOS: allene oxide synthase; EDS: lipase-like proteins; PAD: lipase-like proteins; ICS: isochorismate synthase; PR: pathogenesis-related; LRR-RP: A kind of cell-surface LRR receptor kinase; BAK1: plant receptor kinase. The SOBIR1 cell-surface LRR receptor kinase links EDS1, PAD4, and ADR1 protein complex formation co-regulates PTI and ETI.
Figure 4. Molecular mechanisms of maize response to Rhizoctonia solani infection. RBOH: respiratory burst oxidase homolog; CNGC: Ca2+ channel protein; POX: peroxidase; PAL: phenylalaninammo—nialyase; POD: peroxidase isozyme; SOD: superoxide dismutase; CAT: catalase; APX: ascorbate peroxidase; GPX: glutathione peroxidase; AOC: allene oxide cyclase; AOS: allene oxide synthase; EDS: lipase-like proteins; PAD: lipase-like proteins; ICS: isochorismate synthase; PR: pathogenesis-related; LRR-RP: A kind of cell-surface LRR receptor kinase; BAK1: plant receptor kinase. The SOBIR1 cell-surface LRR receptor kinase links EDS1, PAD4, and ADR1 protein complex formation co-regulates PTI and ETI.
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Figure 5. The ways to control and prevention of sheath blight disease of maize.
Figure 5. The ways to control and prevention of sheath blight disease of maize.
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Table 1. History of sheath blight research and important progress.
Table 1. History of sheath blight research and important progress.
YearEventReferences
1903Rhizoctonia solani was first identified.Rolfs et al. [4]
1966The earliest records of the occurrence of corn sheath
blight in China were found in Jilin Province.		Qi et al. [5]
1952Studies on the efficacy of disinfectants (formaldehyde and sublimate) on the vitality of Rhizoctonia solani Kuehn were conducted.BŁASZCZAK W et al. [6]
1982The occurrence and control strategy of maize sheath blight were first proposed in China.Xie et al. [7]
1995The quantitative trait loci (QTLs) in cultivated rice contributing to field resistance to sheath blight (Rhizoctonia solani) were characterized for the first time.Li et al. [8]
2005Three major QTL sites for the resistance index of maize sheath blight were detected for the first time.Yang et al. [9]
2011The mechanism behind the increased resistance of maize to sheath blight was reported for the first time.Song et al. [10]
2019The negative feedback regulatory resistance gene FBL41 was cloned from maize for the first time, and a new mechanism by which the gene product enhances the plant’s disease resistance by regulating the synthesis of lignin, an important component of cell wall, was reported.Chu et al. [11]
2022A transcriptome analysis revealed the genes potentially related to the resistance of rhizoctonia contrasticum in maize, providing support for marker-assisted breeding for disease resistance.Cao et al. [12]
Table 2. Disease-causing and resistance-related genes.
Table 2. Disease-causing and resistance-related genes.
TypeGene NameReferences
Disease-related gene
(Rhizoctonia solani AG1-IA)		Endocellulaseeg45-1, eg45-2, eg12Li et al. [18]
Endopolygalacturonaseendo-pg1, endo-pg2, endo-pg3
Exo-cut polygalacturonaseex-pg
Proteasepr-1, pr-2, pr-3, pr-4
Xylanasexyn-1, xyn-2
Cell-wall-degrading enzymesPG, PMG, Cx, PGTE, PMET, FPAYang et al. [19]
Resistance-related geneReceptor kinaseZmWRKY76, ZmWRKY79Gao et al. [20]
Fu et al. [21]
F-box domain-containing proteinZmFBL41Chu et al. [11]
NAC transcription factorZmNAC41, ZmBAK1Cao et al. [22]
Gamma-aminobutyric acid transaminasZmGABA-TGuo et al. [23]
Table 3. QTL mapping studies for resistance to sheath blight in maize.
Table 3. QTL mapping studies for resistance to sheath blight in maize.
ChromosomeMarkerLinked MarkerNumber of QTLs
1SSRumc1245, bnlg1597, bnlg1671, bnlg421, umc1044, umc1321, bnlg1953, bnlg0176, bnlg1203, umc1988, dupssr12, umc2189, bnlg2123, umc179714
2SSRumc1285, umc2150, umc2246, phi96100, bnlg1017, umc1185, bnlg1018, bnlg1036, nc003, umc1658, umc2192, umc1080, dupssr25, bnlg1662, bnlg1721, bnlg1606, bnlg194017
3SSRumc1010, bnlg1350, bnlg197, umc1052, bnlg1447, bnlg1523, bnlg1325, bnlg1456, mmc0022, umc1528, umc165911
4SSRumc2287, phi093, bnlg1755, umc1008, umc2281, bnlg1621, umc1294, umc1662, bnlg1937, bnlg1265, umc1228, bnlg1318, umc2082, umc2081, umc2280, nc005, umc1088, umc1299, umc2137, bnlg0292, umc1051, bnlg2162, bnlg0589, bnlg1890, ZmFBL4125
5SSRumc2307, umc1253, umc1496, umc1416, nc007, bnlg1879, phi10918, umc2164, bnlg1237, umc107210
6SSRbnlg1006, bnlg161, umc1002, bnlg1600, bnlg1538, umcl006, umcl083, 1mc1818, umc1723, umc1257, umc1014, umc2318, umc1187, umc1859, bnlg1443, bnlg1759, umc205917
7SSRbnlg1686, phi116, umc1428, bnlg2132, umc1016, bnlg1792, bnlg2203, bnlg1305, bnlg1805, dupssr13, umc1154, bnlg1759, umc205911
8SSRphi123, umc1034, bnlg1834, umc1858, bnlg0666, umc1960, umc2357, bnlg10568
9SSRumc1231, bnlg1583, dupssr06, bnlg1714, umc23435
10SSRumc1152, umc1319, phil18, mmc0501, phi054, umc1993, bnlg1518, bnlg11858
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Di, R.; Liu, L.; Shoaib, N.; Xi, B.; Zhou, Q.; Yu, G. Sheath Blight of Maize: An Overview and Prospects for Future Research Directions. Agriculture 2023, 13, 2006. https://doi.org/10.3390/agriculture13102006

AMA Style

Di R, Liu L, Shoaib N, Xi B, Zhou Q, Yu G. Sheath Blight of Maize: An Overview and Prospects for Future Research Directions. Agriculture. 2023; 13(10):2006. https://doi.org/10.3390/agriculture13102006

Chicago/Turabian Style

Di, Runze, Lun Liu, Noman Shoaib, Boai Xi, Qiyan Zhou, and Guowu Yu. 2023. "Sheath Blight of Maize: An Overview and Prospects for Future Research Directions" Agriculture 13, no. 10: 2006. https://doi.org/10.3390/agriculture13102006

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