Tomato (Solanum lycopersicum L.) is one of the ubiquitous and vital crops grown worldwide (Howladar, 2016; El-Sappah et al., 2021a; Abbas et al., 2022). The fruit’s appealingness (sizes, colors, flavors, and forms), widespread use, and synthesis of the medicinal chemicals contribute to an annual increase in consumption (Cheng et al., 2020). Tomato fruits are significant because they provide dietary fiber, antioxidants, vitamins, minerals, proteins, carbohydrates, and other nutrients needed for a healthy human diet (Liu et al., 2020; Alluqmani and Alabdallah, 2022). On the other hand, tomato plants are vulnerable to several ailments, and approximately there are 136 viral species known to be harmful (Qi et al., 2021; Islam et al., 2022).

One of the most severe viral diseases to plague tomato plants is tomato yellow leaf curl virus (TYLCV), brought by a group of phylogenetically related Begomovirusspp, and spread by the whitefly Bemisiatabac (Piedra-Aguilera et al., 2019). TYLCV symptoms in tomato plants are hindered development, chlorosis, leaf curl, and powerless natural product yield (Lapidot and Polston, 2006). In 1932, the TYLCV virus was discovered for the first time in Sudan and the Middle East (Idris and Brown, 2005; Van Brunschot et al., 2010). It has since spread throughout the world’s tropical and subtropical regions, including the Mediterranean Basin, the Far East (Asia), the Caribbean, Australia, North, South, and Central America, and many others ( Figure 1 ) (Czosnek and Laterrot, 1997; Navas-Castillo et al., 1997; Zhang et al., 2009; Péréfarres et al., 2010; Ning et al., 2015; Kil et al., 2016). Recently, it was discovered that TYLCV was seed-distributed (Kil et al., 2016; Kil et al., 2017; Kil et al., 2018). However, the vector Bemisiatabaci (Gennadius) (Hemiptera: Aleyrodidae), notably biotypes B and Q, are responsible for the majority of diseases during transportation (Pan et al., 2012) by the whitefly in its adult stage, Bemisiatabaci, possibly the most bothersome pest of vegetables and other produce (Ning et al., 2015; Pakkianathan et al., 2015).

Diverse methodologies have been utilized to hinder the spread of TYLCV, including strict quarantine guidelines, traditional rearing, and hereditary designing (Lapidot and Polston, 2006; Polston and Lapidot, 2007). Till today, cultivated tomato varieties have included the Ty-1 to Ty-6 resistance genes from their related species, which has resulted in the development of virus resistance, but it’s crucial to emphasize that this resistance has never been entirely effective (Prasad et al., 2020; Yan et al., 2021; Mori et al., 2022). Ty-1, Ty-2, Ty-3, and ty-5 have all been cloned in recent years (Ren et al., 2022). Ty-1, Ty-3, Ty-4, and Ty-6 genes were all introduced from S. chilenseaccessions and are located on chromosomes 6, 6, 3, and 10, respectively (Zamir et al., 1994; Ji et al., 2007a; Ji et al., 2009b; Kadirvel et al., 2013; Tabein et al., 2017; Gill et al., 2019). The ty-5 and Ty-2 were introgressed from S. peruvianum and S. habrochaites, respectively (Hanson et al., 2006; Hutton et al., 2012). Ty-1 is an allelic variant of Ty-3 that codes for an RNA-dependent RNA polymerase; it is the first resistance locus discovered in S. chilense (LA1969) (Verlaan et al., 2013). The Ty-1 can make geminiviruses more resistant by boosting the viral genome’s cytosine methylation (Butterbach et al., 2014). The Ty-2, a dominant resistant gene on chromosome 11, can confer resistance to some monopartite begomoviruses, including TYLCV, but not to any other monopartite or bipartite begomoviruses like Tomato yellow leaf curl Sardinia virus (TYLCSV) (Barbieri et al., 2010; Prasanna et al., 2015). Ty-4 confers resistance to TYLCV less effectively than Ty-3, which was delivered by introgression from the long arm of chromosome 3 of S. chilense (LA1969) (Ji et al., 2009b). The tomato homolog of the messenger RNA surveillance factor Pelo, implicated in the ribosome recycling phase of protein synthesis, has recently been linked to the ty-5 gene (Anbinder et al., 2009), located on chromosome 4 of S. peruvianum (Lapidot et al., 2015). The Ty-6 gene confers resistance against monopartite and bipartite begomoviruses, completing the protection provided by the known Ty-3 and ty-5 genes (Gill et al., 2019).

The resistance breakthrough fueled the TYLCV dispersion, prompting plant breeders to continually search the wild tomato gene pool for potent new sources of resistance. Immunization schedules, screening and validation of resistance sources, gene discovery and genetic mapping, field evaluation of resistance gene transfer to cultivars and inbred lines, global dissemination, TYLCV symptoms, and immunization techniques are all part of TYLCV resistance breeding programs. The presentation will focus on innate immunity to TYLCV, organized resistance genetic defense, marker-assisted resistance breeding selectable markers, and natural resistance resources. The main objective is to lay the background for future studies into the genes responsible for TYLCV disease resistance.

Earlier study shows that the whole tomato plants were weakened by TYLCV infection, and there was a significant decrease in the yield. After inoculation, the first TYLCV symptoms on tomato plants appear 2-4 weeks later and may take up to two months to fully manifest (Ioannou, 1985). The virus isolates, host genetic background, ambient conditions, development stage, and physiological state of the tomato plant at the time of infection influence the kind and intensity of symptoms (Mauck, 2016). The leaflets of newly emerged leaves curl downward and inward in a hook-like pattern early after infection (Salati, 2001) ( Figure 2 ). Afterward, leaves are distorted and narrower with chlorosis in the center and edges and leaflet margins curling upward (Vallad et al., 2018). The underside of leaflets may also be stained purple (Gorovits et al., 2013; Ibne-Siam-Joy, 2020).

Temperatures exceeding 25°C can aggravate leaf symptoms (Polston and Lapidot, 2007; Anfoka et al., 2016). Infectious plants showed severe symptoms such as yellowing, curling, and a significant loss in apical leaf size (Lapidot et al., 2001). The leaves curl between the veins, and the midrib may become arched And thepetioles twisting can be seen in elder leaves (Shankar et al., 2014). The leaf surface was found to have pale yellow dots that grew larger with time (Gorovits et al., 2013) which is, however, a less prevalent symptom. Tomato plants contaminated with TYLCV were significantly stunted, with numerous branchlets and reduced internodes (Davino et al., 2006; Shankar et al., 2014). Due to increased flower shedding, young, early-affected plants are frequently infertile. Since most blooms (>90%) droop after infection, there is almost no fruit. As a result, yield reductions are more significant when plants are infected prematurely. Late-stage infections can drastically diminish the yield of new fruit. Infected plants produce fewer and smaller fruits that come off easily. Fruit ripens appropriately and is likely to bear before infection (Dam et al., 2005).

In vivo and in vitro approaches are used to test the rate of TYLCV infection and understand the processes of plant resistance to TYLCV as shown in Figure 3 .

Natural TYLCV-resistant germplasm resources have been studied and characterized in numerous tomato lines, genotypes, and cultivars over the last few decades, most of which are addressed in Table 1 . S. pimpinellifolium, S. peruvianum, S. chilense, S. habrochaites, and S. cheesmaniae are wild tomato that have been the focus of plant breeders’ efforts to uncover natural sources of virus resistance (Yan et al., 2018). Ty-1’s initial source was LA1969, (Verlaan et al., 2011; Verlaan et al., 2013) and Ty-2 from S. habrochaites f. glabratum accession “B6013” (Yang et al., 2014). The self-incompatible and heterogeneous S. chilense wild tomato variety produces numerous alleles of the same gene in a single accession (Bai et al., 2004). LA1932 demonstrates that resistance allele 35 exists for Ty-1/Ty-3 and Ty-4 (Ji et al., 2009b). In LA2779, Ty-3 and Ty-6 were also discovered (Hutton and Scott, 2013). The potential that previous S. chilense-derived lines carry various resistance genes for TYLCV resistance in accordance with the selection process and heterogeneity of S. chilense (Caro et al., 2015). Finally, several tomato varieties and cultivars have recently been introduced around the world through various breeding programs, such as Yarkiy (Rumyanets), Malinovyi (Slon), and Nicola in Kazakhstan (Pozharskiy et al., 2022). Quamruzzaman et al. (2021) evaluated 75 tomato entries in Bangladesh for resistance to TYLCV infection, and 47 showed zero percent infection. Furthermore, in Egypt, two new tomato lines (TYG-1-3 and KIS-N-2-1) were resistant to TYLCV infection (Elmorsy et al., 2021). Hussain et al. (2022) screened 24 lines in Pakistan for TYLCV using disease scoring and TAS-ELISA; seven accessions, Acc-17890, AVR-261, CLN-312, AVR-321, EUR-333, CLN-352, and CLN-362, expressed resistance to TYLCV.

Six distinct genes (Ty-1, Ty-2, Ty-3, Ty-4, ty-5, and Ty-6) are located on different tomato chromosomes ( Figure 4 ) and provide varying levels of resistance in wild germplasm when transfected into commercial cultivars (Anbinder et al., 2009; Hutton and Scott, 2013; Prabhandakavi et al., 2021). Except for ty-5, which has recessive inheritance, all of these genes are dominant resistance (Ren et al., 2022). Ty-1, Ty-3, Ty-4, and Ty-6 are derived from S. chilense (Hutton and Scott, 2013), whereas Ty-2 and ty-5 may be derived from S. habrochaites and S. peruvianum, respectively (Anbinder et al., 2009; Wolters et al., 2015). It is now possible to introduce resistance genes without causing cross-resistance or to pyramid numerous resistance genes in marker-assisted breeding thanks to the development of molecular biotechnology.

Indirect selection of desirable plant phenotypes employing linked molecular DNA markers as a binding mechanism is known as marker-assisted selection (MAS) (El-Sappah et al., 2019; El-Sappah and Rather, 2022). According to the MAS theory, a gene of interest is present when a closely connected marker is found (Jiang, 2013). The development of novel resistant crops has numerous advantages. The two main benefits of molecular breeding are that it takes less time (Xu and Crouch, 2008) and is less expensive than field screening (Morris et al., 2003). Additionally, it is less damaging to the environment than pesticides (Afify et al., 2022). The tomato is one of the most remarkable plants for commercial breeding with molecular markers (Hanson et al., 2016). Molecular markers for MAS in CAPS and SCAR markers have been used to develop the Ty-1/Ty-3 resistance gene (Ji et al., 2009a; Nevame et al., 2018; Kim et al., 2020). Although, concerns have been voiced over their physical proximity to the resistance genes in the genome, posing the possibility of false-positive or false-negative outcomes in breeding programs (Antignus, 2007; Yang et al., 2014; Nevame et al., 2018). Gene-specific marker technology was developed to create gene-specific molecular markers to get around the issues mentioned earlier (Ramkumar et al., 2010; Ramkumar et al., 2011). As a result, functional markers, resistance gene-based markers (RGM), gene-targeted markers, and RNA-based markers have all been developed (Sorri et al., 1999; Kasai et al., 2000; Valkonen et al., 2008). Functional markers are polymorphic DNA sequences that play a role in phenotypic trait variation, according to Andersen and Lübberstedt (2003), whereas gene-targeted markers are gene-specific and can mark untranslated regions (Arnholdt-Schmitt, 2005; Varshney et al., 2007). RGM can make it possible to detect resistance genes in fresh germplasm and isolate populations to support plant gene pyramids (Poczai et al., 2013). The DNA markers for these TYLCV resistance genes are presented in Table 2 . Since Ty-1 and Ty-3 were discovered separately from various tomato germplasms, various DNA markers closely related to Ty-1 or Ty-3 have been applied in tomato breeding projects. However, new research has revealed that these two are allelic-related at a single locus (Verlaan et al., 2013; Caro et al., 2015). Research is being done on the resistance levels and spectra that Ty-1 and Ty-3 bestow. Ty-2 resistance was successfully selected using the SCAR marker T0302 on chromosome 11, but it has recently been reported in a 300 kb region, and efforts are being made to identify its genes in order to create gene-based markers (Wolters et al., 2015). Based on the information provided by Lapidot et al. (2015), a gene-based dCAPS marker for ty-5 was developed.

The tomato plant’s molecular and cellular responses to TYLCV infection are depicted in Figure 5 . Six partially overlapping open reading frames are present in the single-stranded, circular, bidirectionally structured DNA genome of TYLCV (Gronenborn, 2007). Due to their restricted coding capability, like most viruses, they depend on the host cell’s machinery and their proteins for the infection cycle (Hanley-Bowdoin et al., 2004). Viral ssDNA exits the capsid and moves into the cytoplasm and nucleus of infected cells, where it engages in a rolling cycle and recombination-dependent replication (Gutierrez, 1999). The freshly replicated viral ssDNA can be transformed into dsDNA, which can be used as a template for further replication or transcription. It can also be encapsulated by viral activity proteins for transport via plasmodesmata from infected cells to nearby cells or packaged in a contagious kind to allow for long-distance viral transmission (Gutierrez, 1999; Hanley-Bowdoin et al., 2013). In addition, geminiviruses rely extensively on host proteins to complete their infection cycle because they have little capacity for coding. To control cell division and the cell cycle, coordinate with multiple cellular mechanisms, and affect host components at various cellular levels, their replication, and transcriptional processes depend on host enzymes (Hanley-Bowdoin et al., 2013). Additionally, they produce short RNAs and block numerous TGS and post-transcriptional gene silencing (PTGS) components by encoding a variety of proteins that disrupt PTGS pathways (Raja et al., 2010; Hanley-Bowdoin et al., 2013; Gnanasekaran et al., 2019). In order to reduce symptoms in different crops and viruses, these proteins also utilize viral suppressors of the RNA silencing mechanism (VSRs) (Ceniceros-Ojeda et al., 2016; Basu et al., 2018). Geminivirus VSRs are versatile proteins that support the viral life cycle and weaken host defense (Teixeira et al., 2021). They can abolish PTGS and TGS in any of the three stages of the operation, and they can also directly or indirectly impact DNA methylation through events that happen after TGS (Loriato et al., 2020). Mechanically, RNA silencing machinery components are either actively inhibited or prevented from accumulating (expression) by geminivirus VSRs. Representatives of the viral repertoire known as C4/AC4 interact with and sequester dsRNA precursors from DCL cleavage and siRNAs from RISC loading in order to prevent antiviral RNA silencing. AC1 (bipartite geminiviruses) and C1 (monopartite geminiviruses) have been shown to function as powerful VSRs in both PTGS and TGS (Amin et al., 2011; Sunitha et al., 2013). Additionally, during the amplification phase, a subsequent event of TGS, AV2 and V2 impair host methylation activity and block antiviral RNA silencing (Luna et al., 2017; Wang et al., 2018a; Luna et al., 2020). Through a number of methods, the C1 protein encoded by the -satellite genome functions as an effective VSRs, preventing the methylation of viral genomes in plants and PTGS that have been infected (Yang et al., 2011; Saeed et al., 2015). To identify and trigger defense reactions against pathogens, the plant immune system has created a multi-layered receptor system. The initial line of defense, according to the traditional zig-zag model of plant immunity, is the recognition of pathogen-associated molecular patterns (PAMPs) by host pattern recognition receptors (PRRs), which activate PAMP-triggered immunity (PTI) (Jones and Dangl, 2006). Successful pathogens release effectors in response, suppressing the PTI response and causing effector-induced susceptibility (ETS). Receptor-like kinases (RLKs) and receptor-like proteins, two transmembrane receptors, are responsible for the appearance of PRRs. These PRRs realize damage-associated molecular patterns (DAMPs), which are exclusively expressed by endogenous danger signals supplied by pathogens or host plants during infection (Macho and Zipfel, 2015). To create an active immunological complex, RLKs and RLPs typically need a co-receptor (Ma et al., 2016). PAMPs and DAMPs function as bonds to enhance the dimerization and oligomerization of PRRs, one-way transmembrane receptors interacting with RLK co-receptors to initiate signaling and activate immune complexes (Macho and Zipfel, 2015). Following PTI activation, the MAP kinase cascade is activated, PTI-related defense genes are induced, ethylene and salicylic acid are synthesized, and callose is deposited (Teixeira et al., 2021; Raza et al., 2022). PTIs appear to be a component of the host’s arsenal of defense against geminivirus infection, despite the fact that geminivirus PAMPs and their associated PRRs have not been described. The TYLCCNB-C1 protein interacts with and is phosphorylated by tomato sucrose non-fermentation 1-associated kinase (SlSnRK1), which may cause proteasomal destruction (Shen et al., 2011). It has been demonstrated that the TYLCCNB-C1 protein inhibits methylation-mediated RNA silencing and its function in lowering PTI in tomato plants. Another line of defense is available. Where plants produce cytoplasmic R proteins, also known as NB-LRRs (nucleotide-binding leucine-rich repeat proteins), which can detect the presence or absence of specific viral impacts, such as avirulent (AVR) activity and result in effector-induced immunity (ETI) (Jones and Dangl, 2006). According to their N-terminal structures, plant NLRs are divided into two groups: CC-NLRs (CNLs) and Toll/Interleukin-1 (TIR)-NLRs (TNLs) (Selth et al., 2004). Ty-2 is a CC-NBS-LRR (CNL) type gene member of the CNL genes with an I-2-like subclass (Shen et al., 2020). When Ty-2 is co-expressed and activated with the TYLCV Rep/C1 protein, a hypersensitive responses (HR) response is produced.

ETIs frequently cause HR and systemic acquired resistance (SAR) (Saile et al., 2020). Recent research suggests that there may not be a very distinct difference between PAMPs and effectors or between PAMP receptors and resistance-causing proteins (Thomma et al., 2011). As a result, PTI and ETI are not always different defensive reactions; instead, both defensive reactions can be strong or weak depending on the contact circumstances. Thus, detecting danger signals, whether they come directly from microorganisms (PAMPs and effectors) or through damage to or change of eukaryotic host structures, can recapitulate the activation of innate plant defense. The geminivirus AC2/C2 protein, a viral effector required for productive infection and can occasionally cause HR, seems to fit these criteria (Roy, 2016).

In general, plant defense responses triggered by direct or indirect effector sensing by NLR genes involve a variety of downstream signaling pathways, including phytohormones involved in defense, MAPK signaling cascades, and a set of defense-related genes (e.g., WRKY transcription factors) (Elmore et al., 2011; de Ronde et al., 2014; Boualem et al., 2016; Rasheed et al., 2022). After TYLCV inoculation, the SlMAPK1, SlMAPK2, and SlMAPK3 were differently upregulated and activated (Li et al., 2017; Guo et al., 2021). Rapid reactive oxygen species (ROS) burst and activation of MPK3/MPK6 are two distinct early signaling events in the plant immune system (Xu et al., 2014; Edris et al., 2021; Elebeedy et al., 2022; Sattar et al., 2022). The SA synthesis can result from H₂O₂ buildup (León et al., 1995); however, TYLCV also promotes SA accumulation early in infection (Morinaka et al., 2006). High SA and H₂O₂ can activate the PR genes expression locally (Peleg-Grossman et al., 2010).

In order to silence the expression of viral genes, geminiviruses must contend with plants on two major defenses. PTGS damages viral mRNA, while methylation-mediated TGS targets viral minichromosomes (Gupta et al., 2021). Geminivirus DNA enters the nucleus after combining with coat proteins and then attaching to the host’s histone proteins; ssDNA is replicated in the nucleus in double-stranded form and exists as minichromosomes (Abouzid et al., 1988; Gupta et al., 2021). The RNA-directed DNA methylation device (RdDM) employs transcriptional gene silencing to silence viral gene expression and reduce viral minichromosomes by taking advantage of the plant’s response to the invasion (TGS) (Vanitharani et al., 2005; Zarreen and Chakraborty, 2020).Virus-produced Plant cytoplasmic siRNA-mediated silencing pathways specifically target RNA transcripts (Gupta et al., 2021). The PTGS pathway is essential for host genes’ expression, development, and defense (Chen et al., 2004).

RDR2 participates in tomatoes’ TGS pathway and antiviral defense (Mourrain et al., 2000; Xie et al., 2001; Qi et al., 2009). Element members of the Ty-3/Gypsy-like superfamily of retrotransposons, which are transcriptionally repressed through the RdDM pathway, are upregulated due to the loss of RDR2 function (Jia et al., 2009). The TYLCV virus has two wild-type tomato resistance alleles, Ty-1 and Ty-3. These alleles are members of the RDR lineage and encode the DFDGD motif (Verlaan et al., 2013; Caro et al., 2015). Other research has demonstrated that Ty-1 increases antiviral RNAi responses, which is implied by elevated vsiRNA levels and elevated cytosine methylation in the viral DNA genome in tomatoes treated with Ty-1 (Butterbach et al., 2014). The viral genome’s cytosine methylation and RNA silencing are hypothesized to be regulated by several Ty genes (Verlaan et al., 2013; Butterbach et al., 2014; Caro et al., 2015).

Finally, autophagy, a conserved evolutionary process that recycles damaged or unneeded cellular components within cells, is another method of plant defense against TYLCV (Haxim et al., 2017; Yang et al., 2019a). According to studies on plant DNA and RNA viruses, autophagy has a potential antiviral role in host innate and adaptive immunity (Hafrén et al., 2017; Haxim et al., 2017; Gupta et al., 2021). The TLCYnV Rep protein CLCuMuB C1 interacts with the autophagy-related protein NbATG8 and regulates its degradation via the ATG8 interaction motif (LVSTKSPSLIK) (Gupta et al., 2021). More research, particularly in tomatoes, is needed to understand how autophagy is regulated during viral infection and determine whether blocking the proviral autophagy pathway could prevent diseases.

The TYLCV may have originated from seeds because viral particles can stay in the seed after infection and pass on to the following generation (Albrechtsen, 2006; Baldodiya et al., 2020). Strict quarantine laws, integrated pest management, and traditional breeding are only a few methods to stop the spread of TYLCV (Prasad et al., 2020). TYLCV transmission is one of several recent transgenic strategies and traditional methods used to combat virus transmission (Pramanik et al., 2021; Asseri et al., 2022). Tomato plants that express TYLCV gene segments, such as replication-associated protein (Rep) (Antignus et al., 2004) or capsid protein (CP) provide resistance to the virus (Yang et al., 2004). Another study found that the model plant N. benthamiana overexpressed recombinant antibodies directed against the Rep protein and displayed decreased TYLCV symptoms (Safarnejad et al., 2009; Reyes et al., 2013). Immunization against TYLCV was successfully developed using viral gene silencing via RNAi-mediated techniques (Ammara et al., 2015; Leibman et al., 2015; Fuentes et al., 2016); for example, viral resistance was demonstrated by silencing the tomato SlPelo gene (Lapidot et al., 2015). Meanwhile, the overexpression of plant immunity-related genes immunity is a reasonable strategy for increasing pathogen tolerance in plants. For instance, SlMAPK3 or SlLNR overexpression reduces TYLCV pathogenicity in tomato plants (Li et al., 2017; Yang et al., 2019b). Furthermore, SlGRXC6 overexpression promoted plant growth, inhibited viral infection, and delayed TYLCV symptom development (Zhao et al., 2021).

Traditional breeding and transgenic approaches to TYLCV infection control are generally promising, but they have several drawbacks. Besides, they have been around for a long time and faces the risk of losing essential characteristics due to traditional breeding domestication (Jansson et al., 2017; Migicovsky and Myles, 2017). The main disadvantage of transgenic techniques is that the transgene must be expressed steadily to achieve a pathogen-tolerant phenotype. Thus the organisms must be classified as genetically modified (GMOs) (Shelake et al., 2019). Plant viruses have also been reported to develop a protection system by developing RNA-silencing viral suppressors (Incarbone and Dunoyer, 2013), even though RNAi does not result in complete gene silencing and requires the components of RNAi to be expressed consistently (Shuey et al., 2002; Rehman et al., 2022). As a result, novel approaches to developing TYLCV-resistant tomato crop varieties are incredibly crucial. CRISPR/Cas technology has proven to be a promising tool for creating designer crop varieties, including pathogen-resistant crops (Shelake et al., 2019; El-Sappah et al., 2021b; Pramanik et al., 2021). The two main components of CRISPR/Cas-based genome editing tools are single guide RNA (sgRNA) and Cas9 endonuclease (Binyameen et al., 2021). The sgRNA-Cas9 complex searches the genome for its target site and uses an adjacent protospacer motif to generate efficient DNA double-strand breaks. During the error-prone DNA repair process, mutations can occur (Pramanik et al., 2021). CRISPR/Cas has recently been used to target either the pathogen genome or the genes of the host plant to achieve a disease-resistant phenotype. By targeting the viral genome, CRISPR/Cas technology is effective in providing TYLCV resistance in N. benthamiana (Ali et al., 2015; Zaidi et al., 2016; Tashkandi et al., 2018). Similarly, sgRNAs targeting the CP or Rep gene decreased TYLCV accumulation in tomato plants (Tashkandi et al., 2018). According to a study published by Pramanik et al. (2021) the commercial tomato BN-86 line was CRISPR/Cas9-interceded to produce TYLCV-resistant tomato plants. Finally, in order to gain viral immunity, targeting the viral genome necessitates the stable expression of the CRISPR/Cas system, and is thus classified as GMO.

The most destructive viral disease that affects tomatoes is likely TYLCV disease. Traditional strategies, such as reproduction and transgenic techniques, have had limited success in controlling the disease. The QTL for TYLCV resistance, including Ty-1, Ty-2, Ty-3, Ty-4, ty-5, and Ty-6 in wild tomato varieties, were only recently discovered. Several methods, including stringent quarantine laws, genetic engineering, conventional breeding, and integrated pest management, have been used to stop the spread of TYLCV. Typically, tomato uses a few defense mechanisms, such as PTI, ETI, Gene silencing, and autophagy, to reduce the dangerous effects of TYLCV infections. This study compiles the characteristics of specific opposition genes, typical opposition resources, subatomic markers for aided choice, and methods for determining TYLCV protection. The main objective is to set the theoretical groundwork for identifying, utilizing, and developing tomato varieties resistant to TYLCV.

Conceptualization: AE-S, JiaL, KY, MA, AS, MASA, XZ and RM. Draw the figures: AE-S and SQ. Collected the data: AE-S. Contributed to writing the original manuscript draft: AE-S. Review and editing of the manuscript: AE-S, QH, G-TC, JinL, LW, JiaL, MI, XZ, MASA, AS and MA. Writing final copy: AE-S, SS, and ZN. All authors contributed to the article and approved the submitted version.