Fungal diseases of eggplant (Solanum melongena L.) and components of the disease triangle: A review

ABSTRACT Eggplant (Solanum melongena L.) is one of the most popular solanaceous vegetable crops cultivated mainly in the tropical and subtropical parts of the world. Eggplant production is challenged by a wide range of pathogens, such as bacteria, fungi, viruses, and nematodes. The fungi cause the most severe economic loss to eggplant farmers due to their widespread incidence and devastating impact on crop yield. The fungal diseases are influenced by several factors, including environmental conditions, physiological and genetic characteristics of the host. Despite the economic implications of fungal diseases in eggplant, a compilation of the current understanding of pathogenesis, disease development and the host-resistance mechanisms remain unavailable. In this article, we comprehensively review common fungal pathogens of eggplant reported worldwide, and the diseases caused by them, including their major symptoms. We also discuss the major environmental factors that favor pathogenesis and summarize the molecular mechanisms underlying the host-pathogen interactions and disease development. Finally, we briefly discuss the prospects for future research to develop modern breeding and agronomic tools for combating the diseases in this important crop.


Introduction
Vegetables play a critical role in the human diet, providing a wide range of nutrients. A balanced inclusion of fresh vegetables in the daily diet can reduce the risk of chronic health conditions (Joshipura et al. 2001). Solanaceous vegetables are protective foods since they are rich in phytonutrients, dietary fibers, minerals, and major vitamins . Featuring some of the most widely consumed vegetables, such as tomato, eggplant, chillies, and peppers, the Solanaceae family is comprised of around 3,000 species, including several herbs, medicinal plants, and industrial crops (Vorontsova and Knapp 2012). Eggplant (S. melongena L.), also known as Irregular shaped black areas on the leaves, sunken lesions with concentric rings on fruits (Witsenboer et al. 1992;Harimoto et al. 2007;Tsitsigiannis et al. 2008, Shafique et al. 2021

Phomopsis vexans
Phomopsis blight/ fruit rot Leaf: Small circular olive-colored spots, later turns darker with black margins.

Phytophthora infestans Phytophthora blight/
Late blight Water-soaked lesions with a green coloration. Expand and turn brown and appear like spots with greenish yellow margin. White spores on the abaxial surface of the infected leaves corresponding to margin around infection. Infected plant emits an unpleasant odor (Singh et al. 2014a

Sclerotium rolfsii
Collar rot/Foot and root rot Belt-like formation at the collar region above the ground. Slowly progresses upwards and white mycelium seen on the infected portion. Plants wilt, and the dried leaves may remain on the plant or entire plant collapses. Rotting of roots leading to stunted growth or collapse of plant (Danhiber, Dhancholia, and Singh 1991) Tomato, common bean, sugar beet, cowpea, peanut

Septoria lycopersici
Septoria leaf spot Small brown spots on the upper surface of the lower leaves, enlarge in size. Spots will be light in colour and subsequently become darker retaining light colour centre with brown colour borders (Delahaut and Stevenson 2004;Tsitsigiannis et al. 2008) Tomato and other solanaceous crops

Verticillium dahliae
Verticillium wilt Chlorosis and vein clearing, necrosis, stunted growth, browning of vascular tissues, ultimately leading to wilting of the entire plant (Tjamos et al. 2000) Tomato, potato, soybean, cotton, lettuce, olives *Since these pathogens have a very wide host range only some of the economically important crop hosts have been mentioned in the table Leveillula taurica Survives on alternate host plants mostly as cleistothecia and the disease is favoured by a temperature of below 30°C. The relative humidity below 20-40% is found to be unfavourable for pathogenesis and disease progression Tomato Guzman-Plazola, Davis, and

Marois 2003
Phomopsis vexans The seed is the main reservoir of the pathogen, can persist in the soil as well as plant debris.
Preformed external wounds essential for the pathogen to enter into the host cell

Eggplant Muneeshwar and Razdan 2012
Favoured by 27-28°C. Maximum disease development-relative humidity 55%. Rohini, Hariprasad, and Niranjana 2016;Islam and Sitansu 1990 (Continued ) Widely adopted practices, such as application of fungicides, increases the cost of cultivation, impart adverse effects on human health, and result in environmental pollution upon excessive usage (Ons et al. 2020;Baite, Khokhar, and Meena 2021). Moreover, fungicide resistance exhibited by the pathogens demands updating the formulations with a broader mode of action (Hollomon 2015;Lucas, Hawkins, and Fraaije 2015). Therefore, developing more sustainable strategies to manage plant diseases is crucial. Plants exhibit inherent resistance mechanisms to combat the infection by pathogens, whereas pathogens continuously evolve to overcome plants' resistance mechanisms. Climate change induces rapid genetic alterations in pathogens, causing the evolution of novel modes of pathogenicity (Chakraborty 2013;He, Zhan, and Xie 2016;Moller and Stukenbrock 2017). Conventional breeding programs have developed varieties that exhibit considerable resistance to some pathogens. However, the rapidly evolving pathogen strains manage to circumvent this resistance, necessitating more sustainable genetic strategies for resistance (Boyd et al. 2013). In the following sections, we discuss the current understanding of the pathogenesis mechanisms of some of the fungal pathogens of eggplant, host-defense mechanisms, and various genes involved in disease resistance against these pathogens.

Mechanisms of pathogenesis
A pathogen can have host-specific or host-independent mechanisms to establish control over the host by suppressing the host's immune responses. The potential of the pathogenic microorganism to infect the plant and cause the disease is called pathogenicity, and the degree of pathogenicity is referred to as virulence (Casadevall and Pirofski 2003). General pathogenetic mechanisms of phytopathogenic fungi involve structures like appressoria and the secretion of cell-wall-degrading enzymes, toxins, growth regulators, and effector proteins (Cheng et al. 2021). Widely reported fungal pathogens in eggplant have been chosen for detailed discussion. The availability of literature regarding the pathogenetic mechanism has also been used as a selection criterion. The details of the pathogenetic mechanisms of 10 fungal pathogens of eggplant are summarized below. The available literature specific to pathogenicity genes in eggplant is limited to studies in Verticillium dahlia; therefore, other crops, including those closely related to eggplant (other Solanaceae members), have been listed in Table 3.
AAL toxin acts on the host endoplasmic reticulum and inhibits eukaryotic sphinganine and N-acyltransferase, disrupting sphingolipid biosynthesis and leading to cell death in the host (Zhang et al. 2016a). AM toxin acts on chloroplasts and the plasma membrane, leading to invagination of the plasma membrane, inhibiting carbon dioxide fixation, vesiculation of grana lamellae,

Vdhex1
Hex1 plays a role in ROS metabolism and resistance to oxidative stress, required both for normal responses to osmotic stress and factors that affect the cell wall and plasmamembrane integrity. Vangalis et al. 2020 (Eggplant) and loss of electrolytes (Otani, Kohmoto, and Kodama 1995). Mitochondrion is the site of action for ACR and AT toxins. ACR toxin exposure results in swelling and morphological alteration of mitochondria, uncoupling of oxidative phosphorylation, changes in membrane potential, and eventually necrosis (Akimitsu et al. 1989). AT toxin increases H 2 O 2 and stress-related compounds such as proline (Yakimova et al. 2009). ACT toxin targets plasma membrane and plasmodesma. AF toxin targets the plasma membrane by increasing the K + efflux, which affects the polarization. Plasma membrane H + -ATPase is also affected indirectly (Meena and S 2019). The AK toxin targets plasmodesma and plasma membrane, resulting in necrosis of the leaves and rapid efflux of K+ from the plasma membrane. Some of the nonhost-specific toxins produced by different species of Alternaria are alternariol (AOH), tentoxin (TEN), and alterotoxin I, II, III (ATX) (Andersen et al. 2015;Lee, Patriarca, and Magan 2015). Toxins are considered important determinants of the pathogenicity and virulence of Alternaria spp. These toxins, especially host-specific ones, can be used as in vitro selective agents for screening host plants for disease resistance at the molecular level.

Botrytis cinerea
The pathogenesis process of Botrytis spp. differs from that of other necrotrophic fungi, as it requires senescent host tissue to initiate infection and complete its lifecycle (Hegedus and Rimmer 2005). The disease cycle begins when the spores are dispersed to the host cell, followed by conidial germination and penetration into the host tissue. The fungus kills the host tissue, thereby facilitating primary lesion formation (on leaves, fruits, stem) and colony expansion, leading to sporulation and dissemination. The fungus secretes cutinase to penetrate the host cell by degrading the cuticle of the host epidermal cells (Prins et al. 2000).
Pectinase is another important enzyme that helps initiate primary infection (Prins et al. 2000). Wu et al. (2010) reported the importance of pectinase and cellulase enzymes in the pathogenicity of Botrytis in tomato plants. Botrytis cinerea has a long list of virulence factors that regulate different pathogenesis steps (Nakajima and Akutsu 2014). The toxin botrydial produced by Botrytis cinerea in the plant tissues showing soft rot symptoms facilitates penetration and colonization (Colmenares et al. 2002). Two groups of nonspecific phytotoxins, sesquiterpene botrydial and related compounds, and botcinic acid and its botcinin derivatives have been identified in the pathogen (Colmenares et al. 2002). Cyclophilin, a virulence factor produced by the virulent strains of Botrytis, is also known to contribute to its virulence and pathogenicity (Viaud et al. 2003). Fernandez-Acero et al. (2007) analyzed and identified 27 proteins from Botrytis cinerea, which might play a role in the virulence of the pathogenic strains.
There are no studies available on the mechanism of pathogenesis of Botrytis in eggplant. The cerato-platenin family protein, cerato-platenin 1 (BcSpl1) from Botrytis cinerea, contributes to the pathogen's virulence, eliciting hypersensitive responses in tomato, tobacco, and Arabidopsis (Frias, González, and Brito 2011). Botrytis adenylate cyclase (BAC) is essential for expressing the complete pathogenicity of B. cinerea in bean plants (Klimpel et al. 2002). Souibgui et al. (2021) reported on the role of Clathrin Heavy Chain (CHC) in the infection process of B. cinerea in French beans, apple, and cucumber. CHC is associated with the secretion of cell death-inducing proteins (CDIPs), proteins associated with reactive oxygen species (ROS) production, and plant cell-wall-degrading enzymes. They are also involved in virulence factors delivery. A novel factor, BcHBF1 (B. cinerea hyphal branching-related factor 1), has been identified to enhance virulence by promoting hyphal development and host penetration in green bean and apple . Pathogenesis-related genes and their functions in Botrytis cinerea are given in Table 3.

Cercospora spp
Cercosporin, a toxin produced by different species of Cercospora, plays a significant role in its pathogenesis (Daub and Ehrenshaft 2000;Tessmann, Charudattan, and Preston 2008;Souza, Herrero, and Daub 2019). The mode of action of this toxin in eggplant has not been reported. Daub and Ehrenshaft (2000) explain the fundamental biology of the toxin in hosts like tobacco, sugarbeet, banana, and coffee. Light activates cercosporin production. Once secreted, the ROS present in the activated cercosporin molecule cause peroxidation of the lipid layer in the host plasma membrane (Daub and Ehrenshaft 2000). The combined action of toxin and ROS leads to host cellular damage, facilitating nutrient leakage and the development of fungal mycelium (Williamson and Scandalios 1993).

Colletotrichum spp
No reports are available on the specific infection mechanism of Colletotrichum in eggplant. Studies on other plants revealed that the infection process of Colletotrichum spp. has four steps: 1. germination, 2. formation of melanized appressoria, 3. appressorial penetration, and 4. invasive growth in host plants (Liang et al. 2021). After coming in contact with the susceptible host plant, the fungus enters the host cell by producing hyphae in between the host's cell wall and plasma membrane, using melanin-containing thick appressoria (Perfect et al. 1999). Once colonization occurs, the pathogen releases enzymes that degrade the cell wall of the host plant. (Miyara et al. 2010). Colletotrichum spp. prefer alkaline pH and accumulate ammonia during pathogenesis to maintain an alkaline environment, activating host-programmed cell death in beans, avocado, and tomato (O'sConnell and Bailey 1988;Alkan et al. 2009;Miyara et al. 2010). Pectinolytic and cellulolytic enzymes also play a crucial role in the pathogenetic mechanism of C. lindemuthianum, with the virulence of different strains correlating with the amount of these enzymes produced by each (Faisal, Kuppusami, and Thiruvengadam 2014).

Fusarium spp
The specific details of the mechanism by which Fusarium spp. infect eggplant are yet to be understood. In general, the pathogenicity of Fusarium spp. is governed by a series of events broadly categorized as adhesion, penetration, and colonization. The symptoms become visible once the process of penetration and the fungal colonization within the host system are completed (Gardiner, Kazan, and Manners 2013). Functional analysis of the genes involved in the pathogenesis process shows that several genes code for enzymes for cell-wall degradation, transcription factors, and proteins required for cell-wall-integrity maintenance, suggesting the importance of these events in the pathogenesis of the fungus (Adhikari et al. 2020).

Phytophthora spp
The mechanisms of pathogenesis of Phytophthora focusing on eggplant as a host have not been studied. Based on the chemotactic attraction (the ability of an organism to sense chemical gradients that surround it), the motile zoospores of Phytophthora come in contact with the host root system and start the infection cycle . The spores settle on the root surface and secret a proteinaceous substance that helps in adhesion and encystment, followed by germination, penetration, and colonization. After colonization, sporangia develop on the root's surface, forming zoospores (Hardham 2001). Extracellular kazal-like serine protein produced by Phytophthora infestans acts against pathogenesis-related protease P69B in tomatoes (Tian et al. 2004). P. infestans suppresses the host's defense response in tomatoes by producing water-soluble glucans (Savidor et al. 2012). Defense enzymes like cysteine and serine proteases, and β -1,3-glucanases are released by the plant to the apoplast to combat the pathogen invasion. Phytophthora blocks such plant enzymes by secreting inhibitors, such as cysteine protease inhibitor EPIC1, reported to be best functional against tomato and potato proteases (Dong et al. 2014). The pathogen secrets glycoside dehydrogenase for degrading phytoalexins, isochorismatases to tamper with host salicylic acid signalling, and berberine bridge enzymes (BBE) that are essential for the formation of benzophenanthridine alkaloids as plants' response to pathogenic attack Liu et al. 2014).
The growth of the Phytophthora is limited to the host apoplast during the biotrophic stages. Phytophthora is a fungal-like organism with a cell wall lacking chitin. This pathogen can evade detection by the host system because it lacks chitin, a major Pathogen Activated Molecular Pattern (PAMP) that helps the plant detect fungi (Leesutthiphonchai et al. 2018). The pathogen is predicted to have around 560 Arg-X-Leu-Arg (RXLRs) effectors and 190 Crinkle and Necrosis effectors (CRNs) located in gene-sparse genomic regions, which will promote disease development by stimulating the susceptibility factors in the host or inhibiting the host-defense pathways (Ah-Fong, Shrivastava, and Judelson 2017). Wang and Jiao (2019) have listed several effectors and their functions, along with the description of how Phytophthora pathogens make use of these effectors to manipulate the host immune system in several tiers mediated by cell protease, phytohormone, mitogen-activated protein kinase (MAPK), cell membrane, RNA, catalase, E3 ubiquitin ligase, endoplasmic reticulum, nucleotide-binding site, leucine-rich repeat (NB-LRR) protein, and also other plant components. Chepsergon et al. (2020) reviewed interesting strategic approaches used by Phytophthora spp. regarding motility, attachment, host-cell-wall degradation, and apoplastic and cytoplasmic effectors associated with pathogenesis. The pathogenesis mechanism of Phytophthora involves the molecular interaction of host and pathogen with respect to effectors and disease resistance via transgenic approaches (Mazumdar et al. 2021). Phytophthora spp. enters the host by "Naifu" invasion (described as surface breach by polarized, non-concentric force generation at an oblique angle, creating stresses) and slicing through the host-plant surface to enter into the system (Bronkhorst et al. 2021). This invasion involves actin-mediated polarity surface adherence and turgor generation and thus enables the Phytophthora to invade the host without any specialized organ or generation of vast turgor (Bronkhorst et al. 2021).

Pythium spp
Pythium, a soil pathogen, employs a nearly similar pathogenetic mechanism in all its host plants. No reports are available on the pathogenetic mechanisms focusing on eggplant as a host. The penetration of Pythium into the host plant is limited to the outermost layers of the root cap and epidermal cells (Levesque et al. 2010). Degradation of the host cell wall and early penetration into the host system by Pythium is achieved by cellulase and pectinase. Pythium lacks enzymes such as cutinases and xylanases that help degrade complex polysaccharide forms (Martin and Loper 1999). Instead, the pathogen can only access easily degradable forms of polysaccharides. Once Pythium has depleted easily degradable polysaccharides, it switches to the reproductive phase of the life cycle (Boudjeko et al. 2006). The wholegenome sequencing of Pythium ultimum revealed the presence of a small gene family of cadherins, proteins involved in cell adhesion (one of the initial steps in pathogenesis), for the first time in a genome other than metazoans (Levesque et al. 2010). Levesque et al. (2010) also reported that 86% of the genes were expressed differentially in the presence of the host plants. RXLR effectors genes play a significant role in regulating the interplay between host and pathogen (Morgan and Kamoun 2007). They are specifically targeted to the host and are reportedly absent in Pythium ultimum and probably all other members of the genus, making them capable of infecting a broad range of host plants (Levesque et al. 2010;Adhikari et al. 2013). However, Ai et al. (2020 have reported the presence of 359 putative RXLR effectors from nine Pythium spp. for the first time, indicating a more complex mechanism underlying its pathogenesis process and broad host range.

Pyrenochaeta lycopersici
Although the specific mechanisms of pathogenesis of Pyrenochaeta lycopersici in eggplant remain unexplored, a few studies have investigated the mechanism of pathogenesis in other solanaceous crops. This fungus produces endopolygalacturonase and exolyase, which are pectin-degrading enzymes (Goodenough and Maw 1974). Endopolygalacturonase is an extracellular enzyme that degrades the cell lamella, causing root-rot symptoms, whereas exolyase is secreted in limited quantities compared to the other enzymes in tomato (Goodenough and Maw 1973). In addition, glucosidases and endo-and exoglucanases facilitate colonization by degrading the host cell wall to absorb nutrients in tomato (Valente, Infantino, and Aragona 2011). P. lycopersici also secretes some unidentified compounds that divert the direction of the root tip growth of the host plant towards the inoculum to facilitate the colonization and necrosis in the root apex (Clergeot et al. 2012).

Sclerotinia sclerotiorum
The penetration of Sclerotinia sp. into the host system is facilitated by enzymes that help in the plant cell-wall-degradation process. Endo-Polygalacturonase (Endo-PG) hydrolyzes the middle lamella, pectin methylesterase demethylates pectin present in the cell wall, xylanase degrades native xylan; cellulases and hemicellulases degrade cellulose, and phosphatidases act on phosphatide components of host plasma membrane. These are some of the enzymes produced by the pathogen (Lumsden 1979). These enzymes play a major role in altering the structural integrity of the plant cell wall, thereby facilitating establishment and pathogenesis (Figure 2).
The entire process of the pathogenesis of the fungus Sclerotinia can be divided into three major phases: 1) Opportunistic/Saprophytic, 2) Pathogenic, and 3) Necrotrophic/Saprophytic (Hegedus and Rimmer 2005). The ascospores germinate on the host tissue in the first phase, followed by pathogen establishment. The second pathogenic phase is separated by two spatial zones -frontal and trailing. In the frontal zone, there is a constitutive expression of Sclerotinia sclerotiorum polygalacturonase 1 (SSPG1), aspartyl protease (ASPS), oligo-galacturonides (OGA), and peptides. The trailing zone shows a low glucose level, high cAMP levels, low pH, and maximal cell-wall degradation. Necrosis is caused by the combined action of oligogalacturonides and peptides released by the frontal zone. The third phase starts with a decrease in the cAMP levels and pH (acidic pH) in the host cell. Subsequently, the MAPK activates the salt-mediated killer protoxin 1 (Smk1), eventually leading to sclerotial development and lifecycle completion (Hegedus and Rimmer 2005). Oxalic acid has been found to play an important role in the effective pathogenesis mechanism of Sclerotinia by suppressing oxidative burst in tobacco (Cessna et al. 2000). Phosphoprotein phosphatase type 2A (PP2A) plays an important role in the pathogenicity and mycelial development of the fungus in Arabidopsis (Erental, Harel, and Yarden 2007). Calcineurin, a signal molecule, is involved in sclerotial development and pathogenesis in Sclerotium sclerotiorum and its inhibition by calcineurin inhibitors FK506, cysclosporin Reduced cell wall −1,3-glucan content and increased susceptibility to cell wall-degrading enzymes were reported as a result of calcineurin inhibition in Arabidopsis during S. sclerotiorum infection. Also increased susceptibility to the glucan synthase inhibitor caspofungin was also observed in the same study (Harel, Bercovich, and Yarden 2006). As a result, calcineurin is involved in sclerotial development and pathogenesis in Sclerotium sclerotiorum and, most likely, other phytopathogens in tomato and Arabidopsis (Harel, Bercovich, and Yarden 2006). Several genes with a potential role in the pathogenesis process of the fungus reported in various host plants have been reported by Xu et al. (2018) in their review.

Verticillium dahliae
Verticillium is a menacing pathogen that is difficult to control under field conditions because of its broad host range and extended survival capacity in soil (Nakahara, Mori, and Matsuzoe 2021). Several genes involved in the pathogenesis process of Verticillium dahliae in eggplant and other related crops have been identified. A recent study found that 62 genes involved in several biological processes showed differential expression in eggplant upon V. dahliae infection (Li et al. 2021). VdNUC-2 (encoding Neurospora crassa nuc-2 homolog), Vta2 (encoding a zinc-finger regulator), and Ave1 (avirulence on Ve1 tomato) have been reported as pathogenicity-related genes in cotton (Zhang et al. 2016b). A list of genes involved in the pathogenesis process of V. dahliae and their specific function are given in Table 3. Pisuttu et al. (2020) studied eggplant's physiological and biochemical responses to V. dahliae infection based on the time from infection and leaf age. Upon infection, the plants showed visible symptoms, such as wilting, necrosis and leaf abscission, and significant damage to the chloroplasts.

Host defense mechanisms
The defense mechanisms in host plants can be widely classified into passive defense and active defense (Agrios 2005). Physical or chemical barriers represent the passive defense and can include wax, cuticle, cell wall, and other structural elements, which constitute the physical barrier, whereas nutrient deprivation, phytoanticipation, and other related events make up the chemical barriers (Saijo and Loo 2020). Active defense is further divided into rapid and delayed active defense (Agrios 2005). Rapid active defense mechanisms include cellular processes that cause membrane fusion, oxidative burst, and cell-wall reinforcement. In contrast, delayed active defense mechanisms include the production of pathogenesis-related (PR) proteins, pathogen containment, and systemic acquired resistance (Shittu, Aisagbonhi, and Obiazikwor 2019). Zhou et al. (2012) screened 14 eggplant cultivars for their resistance against Verticillium dahlia; enzyme activity was correlated with the host resistance against the pathogen. The levels of phenylalanine ammonia-lyase, polyphenol oxidase, and peroxidase showed a significant positive correlation with the host-resistance levels against the pathogen. Furthermore, exposure to elicitors like chitosan, salicylic acid, methyl jasmonate, and methyl salicylate resulted in elevated levels of lignin, phenolics, and defense-related enzymes in eggplant and the high levels of phenolics and lignin accumulation and increased level activity of key defensive enzymes might help eggplant develop practical and effective resistance against pathogens (Mandal 2010).

Genes involved in disease resistance
The ability of a host plant to resist the growth or establishment of a pathogen is known as resistance (Agrios 2005). Phytopathogenic fungi seize the photosynthetic products and tamper with the host machinery to survive and reproduce. Hence, the host plants have evolved resistance mechanisms to withstand individual or combinatorial biotic stresses (Lu and Yao 2018). It has been established that at least two possible resistance mechanisms are in operation in plants: 1) resistance to control pathogen multiplication and 2) tolerance through the host minimizing the harmful effects of toxins/effectors generated by the pathogens (Roy and Kirchner 2000;Little et al. 2010). Most host-plant genes confer resistance and encode members of the nucleotidebinding site leucine-rich repeats (NBS-LRR) family of proteins (Dangl and Jones 2001;Zhuang, Zhou, and Wang 2012). Dev, Poornima, and Venu (2018) have characterized and phylogenetically analyzed these NBS-LRR genes in wild relatives of eggplant (Solanum nigrum, Solanum violaceum, and Solanum mincanum). Comparing transcriptomes of Solanum melongena L. and Solanum torvum (Sw), 621 and 815 resistance genes were identified in the wild relative (Sw), indicating varied disease resistance mechanisms in these plants (Yang et al. 2014). The introduction of the arginine decarboxylase (adc) gene (that converts arginine into putrescine) enhanced resistance to fungal infections and other abiotic stresses in eggplant (Prabhavathi and Rajam 2007). Three eggplant germplasms (LS1934, LS174, and LS2436) have been found to be highly resistant to Fusarium in previous studies (Miyatake et al. 2016). The genetic mapping of a resistance locus in cultivated eggplant against Fusarium oxysporum f. sp. melongenae identified two alleles Fm1 L and Fm1 E derived from Fusarium-resistant eggplant materials LS1934 and Eggplant parental line 1 (EPL-1) (Miyatake et al. 2016). Collonnier et al. (2001) and Rotino, Sala, and Toppino (2014) have discussed the advancements and critical achievements in eggplant breeding programs, information  Table 4. The overexpression of microRNA miR395 increased eggplant susceptibility to V. dahliae infection by modulating the synthesis of glutathione, which is a cellular protectant and antioxidant defense against oxygen radical-mediated injury caused by pathogens (Mu et al. 2018). The transgenic eggplant lines expressing the glucanase gene from alfalfa showed improved resistance against fungal wilt caused by V. dahliae and F. oxysporum (Singh et al. 2014b). The transcriptome analysis of wild eggplant S. aculeatissimum showed differential expression of some of the V. dahliae resistance-related genes during infection (Zhou et al. 2016). Similarly, four genes Cf-2,  in tomato reportedly confer resistance against Cladosporium fulvum, and V. dahliae (Jones et al. 1994;Song et al. 2017). Gibberellininsensitive dwarf1B (GID1B), a receptor (The GID1 is a soluble GA receptor binding to bioactive gibberellic acids), plays an important role in eggplant resistance to V. dahliae infection . It was suggested that GID1B works with signal pathways that include gallic acid, jasmonic acid, salicylic acid, and Ca2+ to respond to Verticillium wilt infection . Xing and Chin (2000) reported that the yeast D-9 desaturase gene in eggplant increased the levels of some fatty acids (16: 1, 18: 1, and 16: 3 fatty acids) and enhanced resistance to V. dahliae infection. Li et al. (2021) identified 62 miRNA-targeted genes induced by V. dahliae and suggested that most of them might be involved in disease resistance in eggplant. Overexpressing genes npr1 (non-expressor of pathogenesis-related protein 1) and cyp77a2 (CytochromeP77A2) increased disease resistance in transgenic eggplants (Wang et al. 2010;Deng-wei et al. 2014). Rfo-Sa1 (resistance to F. oxysporum f. sp. melongenae from Solanum aethiopicum 1) locus confers total resistance to F. oxysporum f.sp. melongenae and partial resistance to V. dahliae in eggplant (Barchi et al. 2018). Apart from the genetic methods, pathogenicity-related proteins (PR proteins), antimicrobial peptides, and immunization have been proposed as attractive methods for inducing disease resistance in eggplant (Alam and Salimullah 2021). Transgenic plants expressing PR proteins confer resistance to the host against pathogens (Ali et al. 2018). Tomato pathogenesis-related protein genes of at least three different families, viz., PR1, PR2, and PR3, which play an important role in protecting the host against the pathogen, were upregulated following infection by Verticillium dahliae (Robb, Lee, and Nazar 2007).

Conclusion and future prospects
Eggplant is an important vegetable crop that is prone to numerous fungal diseases that devastate crop production. In this review, we have undertaken a detailed compilation of the available information on fungal infections affecting eggplant and the components of the disease triangle -host, pathogen, and environment. There are limited studies on eggplant; therefore, other closely related crops, have been considered. We have provided an account of different diseases and the associated fungal pathogens, including brief insights into their mechanism of pathogenesis and the environmental factors conducive to the infection. We have also discussed disease resistance mechanisms in the host plant, and the host genetic components that confer resistance against fungal pathogens.
Despite the consensus regarding the adverse impact of fungal diseases on eggplant, well-documented statistical data are lacking on the economic loss caused by these diseases to the producers and the cumulative area under cultivation that has faced severe infection by these diseases. Those data are key to categorizing these diseases based on their severity and prioritizing them for research and management. An agriculture field is a highly heterogenous system under the constant influence of many factors. Therefore, studying the pathogens in isolation or their interaction with hosts under controlled environments will not reveal the complete picture unless the dynamic changes in the environmental parameters are also considered. It is important to delineate the effects of varying environmental factors on each pathogen in the context of different hosts. Also, the genetic potential of disease resistance in the host plants can be appropriately evaluated only when tested under the influence of all possible environmental variations. The intricate interactions between various pathogens, host genes, and the environment are poorly explored in the case of eggplant. Understanding these aspects will be fundamental in developing disease-resistant varieties in the future that can perform well under different agronomic conditions. Although chemical methods remain the most commonly adopted practice to curtail the effects of fungal diseases, resistance breeding has been considered a more sustainable mode of disease control in combination with other integrative disease-management methods.
In eggplant, traditional resistance breeding efforts through gene introgression from wild species tend to focus on a few diseases and need to be widened to other diseases. In addition, employing metabolomic, transcriptomic, and genomic approaches will help in investigating the mechanisms of pathogenesis and host response (Kliebenstein 2012). Together, an in-depth understanding of the pathogens and their specific interactions with different host plants are crucial for filling the knowledge gaps and devising specific and effective management strategies. Adhikary, M. C., H. A. Begum, and M. B. Meah. 2017 (12)