Keywords

13.1 Introduction

Soybean (Glycine max) is an important legume crop recognized for its high seed protein and oil content (Chander et al. 2019). Having diverse climate adaptability and high protein content, it is cultivated in most part of the globe. A variety of food products and industrial food items are made from soybeans; in addition, it is also utilized as animal feed (Ratnaparkhe et al. 2022). In India, soya bean (Glycine max (L) Merrill) has been the most cultivated oil seed crop in terms of both production and area since 2005 (Gawai and Mangnalikar 2018). Soybean seeds are high in protein, oil, vitamins, and minerals, and they are an excellent source of vegetable oil and nutritious plant protein (Patil et al. 2018). Soybean accounted for 42% of total oil seed production in India and 25% of edible oil production. In India, soya bean is primarily produced in Madhya Pradesh, Maharashtra, Rajasthan, Karnataka, Telangana, Chhattisgarh, Nagaland, and Gujarat during a kharif season crop (Gawai and Mangnalikar 2018). According to Tripathi et al. (2022), about ten of the total number of fungal pathogens are consistently present in different regions of the world. Six of which are harmful particularly in India, namely, Sclerotium rolfsii, Macrophomina phaseolina, Colletotrichum truncatum, Phakopsora pachyrhizi, Cercospora sojina, and Cercospora kikuchii. Most of the diseased plants are treated with various chemicals to protect the crops and left their residual effects to the environment. It is better to find some resistant genotypes rather than using hazardous chemicals. Although identification of disease-resistant cultivar is difficult task, the modern molecular breeding tools could increase the efficiency to develop disease-resistant cultivars by transferring resistant gene to the genotype of our interest, developing mapping population, identification genomic regions/QTLs, etc. The resistance nature in soybean was found to be monogenic or polygenic (Tripathi et al. 2022). The present study offers a glimpse into the genomic strategies used to identify the genes/markers linked to the targeted genes in soybeans that are resistant to fungal diseases.

13.2 Soybean Rust (SBR), Its Causal Organism, Important Symptoms, and Economic Loss

In the southern hemisphere, primarily in Asia (Taiwan, Thailand, Japan, and India), Africa, and South America, a potentially fatal foliar disease caused by two meticulously associated obligate fungal species, Phakopsora pachyrhizi Sydows and P. meibomiae (Arthur), is posing a serious threat to soybean cultivation (Langenbach et al. 2016). The specific ability of P. pachyrhizi to infect a wide variety of crop species, a total of 95 plants from 42 genera of the family Papillionaceae, presents significant management issues for soybean rust disease (Bromfield 1984). This disease has varying impact on soybean output as it may cause up to 80% yield loss in the zones favourable for growth and proliferation of the causative organism (Hartman et al. 2005).

13.3 Rhizoctonia Root Rot, Its Causal Organism, Important Symptoms, and Economic Loss

Rhizoctonia root rot is a soil-borne fungal disease caused by Rhizoctonia solani Küuhn. It causes up to 60–70% yield losses in India, 30–60% yield losses in Brazil, and 30–45% yield losses in the USA (Ciampi et al. 2008).

13.4 Brown Stem Rot (BSR), Its Causal Organism, Important Symptoms, and Economic Loss

The soil-borne fungus Cadophora gregata is the primary cause of BSR, a serious disease of soybeans (Harrington and McNew 2003). The fungus prevents water and nutrients from moving through the stem of soybean plants, which is essential for their normal growth and development. The majority of BSR illness cases are only detectable after complete pod formation (McCabe et al. 2018). Nutrient deficiency is the most common diagnosis for this illness. Recently, McCabe and Graham (2020) presented a diagnostic strategy based on genes and their network for quick and precise identification to combat misidentification of BSR. The management of this condition may benefit from this strategy. BSR has been cited as the cause of a 38% yield reduction in soybean harvests (McCabe et al. 2018).

13.5 Powdery Mildew (PMD), Its Causal Organism, Important Symptoms, and Economic Loss

The fungus Microsphaera diffusa (Paxton and Rogers (1974) causes powdery mildew. The main signs of this illness are infected soybean leaves that have a white, powdery coating. The rate of photosynthesis is decreased by more than 50% as a result of this coating (Dunleavy 1978). In addition, approximately 35% yield reduction occurs along with deteriorated soybean seed quality (Phillips 1984). The powdery patches are first visible on the leaves, but after a few days, they quickly cover the entire leaf and defoliate (Silva 2004).

13.6 Fusarium Wilt (FW), Its Causal Organism, Important Symptoms, and Economic Loss (FW, Also Known as Sudden Death Syndrome, SDS)

For the first time, wilted soybean plants were diagnosed in May 2014 in commercial fields at Osijek (Slavonia County) and are caused by the fungal pathogen Fusarium oxysporum Schlecht. emend. Snyder and Hansen (Duvnjak et al. 2016). The symptoms of wilting in soybean plants were interveinal chlorosis of leaves, mortality of shoots, and external and internal browning at the base of stems but no symptoms in roots. Due to SDS, yield reductions of up to 5–15% have been seen in the USA (Luo et al. 2001). Due to the disease’s frequently environment-sensitive, unpredictable, and irregular disease appearance as well as its time-consuming and expensive treatment, sudden death syndrome resistance is difficult to control in the field (Gibson et al. 1994). Resistance to SDS is partial, and partial disease resistance has advantages over total resistance in terms of consistency and yield compatibility (Yuan et al. 2002).

13.7 Downy Mildew, Its Causal Organism, Important Symptoms, and Economic Loss

Soybean downy mildew (SDM) is one of the major fungal diseases caused by Peronospora manshurica (Dong et al. 2018). The onset of symptoms is greatly influenced by the environment and is favoured by high humidity and temperatures of 20–22 °C (Phillips 1999). According to Taguchi-Shiobara et al. (2019), 33 different downy mildew races have been identified so far in the USA. In epidemic years, the average yield loss ranged from 6 to 15% (Dong et al. 2018).

13.8 Anthracnose, Its Causal Organism, Important Symptoms, and Economic Loss

The common soybean disease anthracnose is brought on by the fungus Colletotrichum truncatum (Schw.) Andrus & W.D. Moore (Sinclair and Backman 1989). The anthracnose disease caused a yield loss of 16–25% in India (Boufleur et al. 2021). Although several other species are also recognized as anthracnose causal agents, C. truncatum has been thought to be the primary cause of the anthracnose disease in soybeans.

13.9 Soybean White Mould (SWM), Its Causal Organism, Important Symptoms, and Economic Loss

One of the most devastating fungal diseases is soybean white mould (SWM) caused by the fungus Sclerotinia sclerotiorum (Lib) de Barry which can be found in southern Canada and the Upper Midwest of the USA (Kandel et al. 2018). According to Koenning and Wrather (2010), SWM causes significant yield losses and ranked fourth from the top 28 soybean producing US states. Sclerotinia sclerotiorum overwinters in resting structures known as sclerotia in the soil and debris (Yang et al. 1998). However, ascospores that initially touch down on fragile plant parts, such flower petals, are what caused infections of soybean in field situations. They become colonized by ascospores, which subsequently move downhill to infect and girdle the main stem, causing the plant to eventually perish. In addition, necrotic leaves, bleached lesions on stems and pods, white fluffy mycelial growth, and the appearance of black sclerotia on the leaves, stems, and pods are the common symptoms of infected plants (Chen and Wang 2005).

13.10 Phomopsis Seed Decay, Its Causal Organism, Important Symptoms, and Economic Loss

Phomopsis seed decay (PSD) of soybean is the primary cause of poor seed quality and causes a significant yield loss in most soybean-growing countries (Sinclair 1993). PSD is more likely to occur in environments that are hot and humid, and it typically gets worse when early maturing cultivars are planted early in the season. Significant symptoms include shrivelled, elongated, or cracked look and a chalky texture, but seed infection is typically asymptomatic.

13.11 Cercospora Leaf Blight (CLB)/Purple Seed Stain, Its Causal Organism, Important Symptoms, and Economic Loss

Cercospora leaf blight (CLB)/purple seed stain is a foliar fungal disease of soybean caused by Cercospora kikuchii (Albu et al. 2016). Reddish patches on leaves are one of the symptoms. Additionally, these hues intensify and cause soybeans to flower too early. Cercospora kikuchii also reduces the marketability, processing potentials, germination, and vigour of seed (Kashiwa and Suzuki 2021). In soybeans, this fungus is the source of causing both Cercospora leaf blight (CLB) and/or purple seed stain (PSS) disease. In contrast to CLB, which affects leaves and petioles, PSS affects seed pods and seeds. A distinctive abrasion with a dark purple colour is one of these signs. The pathogen’s synthesis of cercosporin led to the development of this lesion (Callahan et al. 1999). Because it degrades the quality of the seed, purple seed stain is a major barrier to its profitable marketability (Li et al. 2019). Various study groups in India have observed yield loss due to purple seed discolouration at different percentages, including 15–30% (Gupta et al. 1999) and 36–80% (Gupta et al. 2014). It is a disease that Americans find undesirable due to economic yield losses (Doupnik 1993).

13.12 Charcoal Rot, Its Causal Organism, Important Symptoms, and Economic Loss

Charcoal rot is caused by soil-borne fungus Macrophomina phaseolina and also causes significant yield reduction in soybean (Tripathi et al. 2022). This disease was first time reported in 1949 in the USA, and it was assumed that the presence of two toxins, phaseolina and botryodiplodin, are responsible for the infection caused by M. phaseolina in crops (Ramezani et al. 2007). M. phaseolina can infect the vascular system by growing and multiplying under favourable environmental circumstances in plants. It obstructs the movement of water and nutrients toward the leaves in the second step, which results in disease symptoms and further premature leaf death (Gupta and Chauhan 2005). Microsclerotia return to the soil after the crop is harvested and remain there for at least 2 years (Reis et al. 2014). Soybean crops have only exhibited little resistance to M. phaseolina (Pawlowski et al. 2015). Due to polygenic inheritance, it is challenging to breed soybean cultivars resistant to charcoal rot (Coser et al. 2017).

13.13 Phytophthora Rot and Stem Rot, Its Causal Organism, Important Symptoms, and Economic Loss

Phytophthora sojae is a soil-borne pathogen that causes Phytophthora root and stem rot diseases. The soybean crop is affected throughout the years by this disease. It is more devastating in flooded areas (Bernard et al. 1957). Phytophthora root rot often results in a yield loss of 35–40%, but under extreme circumstances, it can even result in a loss of 100% of the crop. The most effective strategy for controlling this disease is the creation of resistant cultivars.

In disease management strategies, it is better to find resistance genes or screening resistant cultivars rather than going for chemical application. Advances in plant breeding techniques, application of molecular markers, identification, and expression analysis of target genes linked to disease resistance have opened multiple ways for the modification of the targeted genomic regions of desired genotypes or cultivars (Fig. 13.1). Here we have attempted to explain integrated genomics for several fungal disease management and identification of some resistant lines/genotypes cultivars (Tables 13.1 and 13.2).

Fig. 13.1
A chart illustrates the genomic approaches for disease-resistant cultivar development. The chart includes conventional breeding, genomics, transgenics approach, gene pyramiding, regulatory process, proteomics, metabolomics, spread breeding, genomic selection, and gene editing.

Different genomic approaches for disease improvement in soybean

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Table 13.1 List of identified genomic regions/quantitative trait loci (QTLs) conferring resistance to various fungal diseases in soybean
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Table 13.2 List of some identified different fungal disease-resistant genotypes/lines/cultivars of soybean developed through various genomic approaches
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13.14 Integrated Genomic Approaches for Developing Resistance Against Fungal Disease in Soybean

13.14.1 Screening and Identification of Soybean Genotype/Germplasm Resistant to Fungal Disease

Screening of different genetic materials like pre-breeding lines, germplasms, accessions, etc. has tremendous importance in search of sources for disease resistance in both fields as well as in laboratory condition.

There have been numerous research organization attempts to screen soybean germplasm for the presence of fungal disease resistance in soybean. Recently, Nataraj et al. (2020) evaluated 225 soybean genotypes and identified five genotypes as highly resistant, and they are EC 538828, EC 34372, EC 457254, AKSS 67, and Karune. In addition to this, the genetics of anthracnose resistance in three F2 populations descended from the resistant parents EC 34372 × JS 95-60, EC 457254 × JS 95-60, and AKSS 67 JS 95-60 which showed that the resistance in all three resistant parents was controlled by two key genes interacting in a complimentary manner. Similar study by Sajeesh et al. (2014) identified DSb 12 as an anthracnose-resistant genotype.

13.14.2 Identification of QTL(S)/Genomic Loci Conferring Resistance to Fungal Disease in Soybean

Biparental mapping populations are made up of a group of individuals resulting from inter- or intraspecific crossing between two parents. Such recombinant lines are mostly used to provide pre-breeding sources for use in crop improvement, and they constitute a potent technique for analysing the genetic underpinnings of complex traits in crops (Tripodi 2021). Recently, Chanchu et al. (2022) reported a single QTL, qSBR18.1, for SBR resistance by evaluating a recombinant inbred line (RIL) population comprising of 108 lines developed from a cross between a susceptible cultivar Sukhothai 2 (SKT2) and CM5.

For BSR, the BSR resistance genes in soybean have been mapped by a number of researchers using marker-assisted breeding. The Rbs3 gene was initially mapped by Lewers et al. (1999) using 320 recombinant inbred lines (RIL) developed from a cross between BSR 101 and PI 437.654. The same study was also verified by Klos et al. (2000) using SSR markers. Later study, SSR markers were used by Bachman et al. (2001) to map the Rbs1 and Rbs2 genes on chromosome 16 in soybean. In addition, Perez et al. (2010) have identified some novel sources of BSR resistance. In further study, the genes conferring resistance to BSR were mapped on chromosome 16. These results led to the conclusion that soybean BSR resistance is caused by just one gene (McCabe and Graham 2020). Using mapping populations developed by crossing the resistant sources “Bell,” PI 84946-2, PI 437833, PI 437970, L84-5873, and PI 86150 with either the susceptible cultivar Colfax or Century 84, three BSR resistant genes, Rbs1, Rbs2, and Rbs3, have been discovered and located on chromosome 16 (Rincker et al. 2016).

For powdery mildew (PMD), according to study, three alleles were present at the Rmd locus on the inheritance of host plant resistance to PMD, and they are Rmd, Rmd-c, and rmd (Lohnes and Bernard 1992). In the soybean cultivar PI 243540, Kang and Mian (2010) found that a single dominant gene contributes to PMD resistance at all stages of soybean plant development. They discovered the gene Rmd PI 243540 from the cultivar PI 243540 to be situated between the SSR marker Sat 224 and SNP marker BARC-021875-04228 over the course of their investigation. The PMD resistance gene Rmd was linked to both markers at distances of 9.6 and 1.3 cM, respectively. The use of genetic markers for molecular characterization and diversity analysis among soybean genotypes for powdery mildew resistance has undergone a number of attempts. SSR analysis was utilized by DeMore et al. (2009) to find PMD resistance gene-linked markers in an F2 population, derived from a cross between MGBR95-20937 IAC-Foscarin 31 and MGBR-46 EMBRAPA 48. In their investigation, two SSRs Sat 366 and Sat 393 were discovered and situated 9.41 cM and 12.45 cM away from PMD resistance genes, respectively. More recently, Zhou et al. (2022) examined adult plant resistance (APR) to PMD in soybean using recombinant inbred lines (RILs) populations created from crossing Zhonghuang 24 (ZH24) and Huaxia 3 (HX3). The outcomes showed that a single dominant locus controlled PMD resistance.

In case of FW, quantitative trait loci have significant role of controlling Fusarium wilt resistance. Studies reported four genes in a cluster with two duos in close proximity or two genes in a cluster with each gene exhibiting pleiotropy are responsible for triggering resistance to Fusarium wilt (Stephens et al. 1993). Another study under greenhouse conditions reported single dominant gene Rfs1 may be responsible for controlling SDS resistance (Hnetkovsky et al. 1996). Similarly, a small number of significant QTLs govern some levels of resistance (Triwitayakorn et al. 2005). Consequently, a number of QTLs may also function as a qualitative locus (Anderson 2012). In same study, the candidate genes QRfs1 and QRfs2 are identified for two loci, and both offered resistance against root infection and leaf scorch, respectively (Anderson 2012). According to Fronza et al. (2004), QTLs on linkage group G conferred nine LGs (A2, C2, D2, F, G, I, J, L, and N) for resistance to root infection (Rfs1). According to Soybase (2010) report, more than 56 records of QTLs for Fusarium wilt in soybean have registered. Similarly, Fronza et al. (2004) reported multiple trait loci for resistance on chromosome number 18 (linkage group G), using four populations of almost isogenic lines and nine DNA markers. In linkage group G, it was hypothesized that three to four genes, namely, QRfs-, QRfs1-, QRfs2-, and QRfs3-rich islands, transfer resistance (Anderson et al. 2014). Similar study reported QTLs, namely, BARC-Satt163, BARC-Satt080, and BARC-Satt307 for resistance that were identified on linkage groups G, N, and C2, respectively (Zou et al. 2005). Recombinant inbred lines with presentations that were environmentally stable and contained all three QTLs for resistance were considerably more resistant than other recombinant inbred lines. With a significant impact on the QTL Rfs1, the SSR marker Satt183 has been found to provide resistance to SDS on molecular linkage group J (Sanitchon et al. 2004). The SSR marker Satt183 has been found to provide SDS resistance (56% variance) on linkage group J. The SSR marker Satt183 found to be most significant robust marker associated with QTL for Rfs1 (Sanitchon et al. 2004).

For DM, 31 quantitative trait loci (QTL) were identified using five populations of RILs, derived from (‘Natto-shoryu’ × ‘Tachinagaha’ (NT), ‘Nattoshoryu’ × ‘Suzumaru’ (NS), ‘Satonohohoemi’ × ‘Fukuibuki’ (SF), ‘Kinusayaka’ × ‘COL/Akita/2009/TARC/1’ (KC), and ‘YR-82’ × ‘Harosoy’ (YH) grown across location and years (Taguchi-Shiobara et al. 2019).

For SWM, the use of molecular markers in conjunction with field studies has opened up new possibilities because they are independent of environmental factors. Recently Kandel et al. (2018) reported ten significant QTLs by single marker analysis that could be used as source of resistance to develop SWM-resistant cultivars. Another study by Moellers et al. (2017) reported 58 SNP-based loci had main effects, and some others had epistatic effects that were related to SWM resistance.

For PSD, employing progenies derived from the cross between resistant cultivar ‘Taekwangkong’ and the susceptible cultivar ‘SS2-2’ yielded two QTLs for PSD resistance under greenhouse condition (Sun et al. 2013).

For purple seed stain disease (PSS), the only partially resistant sources for PSS that have been reported are PI 80, 837, and SJ2 (Roy and Abney 1976; Ploper et al. 1992). According to Jackson et al. (2006), a single dominant gene Rpss1, on linkage group G, was shown to be responsible for resistance to C. kikuchii in the cultivar PI80837. In this study, the potential resistant gene was located between the flanking markers Sat 308 and Satt594 away from resistant genomic loci of 6.6 cM and 11.6 cM, respectively, on linkage group G. The use of such molecular markers in PSS resistance study will aid the advantages in marker-assisted breeding and selection (Jackson et al. 2008). Similarly, two SSR molecular markers Satt115 and Satt340 that are associated with resistance of purple seed stain have been identified in an association mapping study by evaluating two population derived from the cross of PI 80,837 (resistant) with AP 350 and MO/PSD-0259 (Alloatti et al. 2015).

For charcoal rot, in a recent study, a total of 140 F2:3 lines derived from the cross PI 567562A (resistant) PI 567437 (susceptible) were genotyped, and QTL mapping analysis revealed one QTL on chromosome 15 and two QTLs on chromosome 16 for resistance to M. phaseolina (da Silva et al. 2019) (Table 13.1).

For Phytophthora root and stem rot of soybean, the mapping of molecular markers conferring resistance to the disease on different linkage groups has advanced since the introduction of the soybean linkage map. Several studies reported different genes responsible for resistance against of P. sojae. The resistant genes Rps1, Rps2, Rps3, Rps4, Rps5, Rps6, Rps7, and Rps8 have been mapped on linkage groups N, J, F, G, G, G, N, and F, respectively, from different studies (Cregan et al. 1999; Sugimoto et al. 2007; Bernard and Cremeens 1981; Demirbas et al. 2001; Buzzell and Anderson 1981; Sugimoto et al. 2011). In addition, one RFLP marker, pT-5, found to be associated with the Rps5 gene (Athow and Laviolette 1982). However, in addition to these resistant genes, soybean also has several partial resistance-related genes (Akem 1996). Some more genomic loci/QTLs have been reported by several researchers and documented which are elaborated in Table 13.1.

13.15 Genome-Wide Association Studies (GWAS) for Identification of Potential Candidate Gene(s) Associated with Resistance to Fungal Disease

With the help of molecular markers, GWAS have been successfully used to understand the genetic architecture of panels of germplasm lines and to pinpoint regions of the soybean genome linked to various disease resistance and also useful for marker-assisted selection in breeding programme. In an association study, 256 germplasm accessions from various countries were examined with several years across the location for their responses to soybean rust (SBR) along with susceptible controls and plant introductions (PIs) with Rpp genes at known loci (Walker et al. 2022). According to GWAS analysis, 31,114 SNPs were found, and 8 significant SNPs in 8 genomic areas on 7 chromosomes were found. Eight genomic areas, including previously unreported parts of chromosomes 1, 4, 6, 9, 13, and 15, as well as the Rpp3 and Rpp6 locus, were found to be related with SBR resistance on 7 chromosomes (Walker et al. 2022). Linkage map analysis with SSR markers revealed significant marker association to rust resistance in the linkage group (LG) C2 in cultivar FT 2 (Cregan et al. 1999). Another study reported a resistance gene situated in between the flanking marker Satt134 and Satt460 on LG-C2 and has been mapped in the cultivar Hyuuga (Monteros et al. 2007). Similarly, Rpp3 was also located at the same location as reported by Hyten et al. (2007). On LG-G, between flanking markers Sct 187 and Sat 064, 1 cM interval has been identified as the location of the Rpp1 locus (Hyten et al. 2007). The Rpp4 locus was located on chromosome 18 in linkage group G by 1.9 cM distance (Silva et al. 2008) and 2.8 cM (Garcia et al. 2008) from SSR marker Satt288, respectively. Meyer et al. (2009) reported Rpp4C4 (PI 459025B) was highly expressed in the resistant genotype, while the expression of the other intrusive genes was essentially undetectable. According to the results of reverse transcription polymerase chain reaction sequencing, Rpp4C4 considered to be the single candidate gene for Rpp4C4-mediated rust resistance. Molecular marker was used to increase the resistance against SBR of Vietnamese elite soybean cultivar (Khanh et al. 2013). In the same study, the Rpp5 gene of SBR resistance was successfully incorporated into a popular Vietnamese soybean variety HL203 by using molecular markers in a backcross breeding technique. The Rpp5 locus was discovered and to be located in the N linkage group between the flanking markers Sat 275 and Sat 280. Further, based on the molecular information, Maphosa et al. (2012) asserted that the three resistance genes Rpp2, Rpp3, and Rpp4 were effectively pyramided in pairwise combinations in the soybean F2 generation.

For Rhizoctonia root rot, the development of resistant genotype was aided by marker-assisted selection in combination with phenotypic selection in later generations. According to an association study, the identified SSR markers, Satt177 on linkage group A2, Satt281 on linkage group C2, and Satt245 on linkage group M, found to be associated with the resistance to Rhizoctonia root rot (Tomar et al. 2011). Utilizing these three SSR markers for further screening revealed the allelic variation for resistance (Sserunkuma 2016). In this study, five alleles were amplified by each of the three markers. These markers amplified uncommon alleles and were found to be highly polymorphic.

For FW, an association mapping strategy by using 282 soybean lines along with 1536 SNP markers was used by Bao et al. (2015) to locate the loci that differ in SDS resistance and were employed, and two new loci were identified on chromosomes 3 and 18. The findings of these studies have accelerated the value of association mapping in locating significant loci in soybean.

For SWM, genome-wide association study revealed a novel QTL on chromosome 1 which is associated with SWM resistance (Boudhrioua et al. 2020).

For charcoal rot, a set of 459 different plant introductions from the USDA soybean germplasm core collection were screened in the field and greenhouse, and GWAS revealed some putative candidate genes led to new source of resistance (Coser et al. 2017). Similarly, in an association mapping study using 130 different soybean varieties and lines, Sat_252, Satt359, Satt190, Sat_169, Sat_416, and Sat460 markers were identified that are associated with the charcoal rot disease (Ghorbanipour et al. 2019).

13.15.1 Virus-Induced Gene Silencing

The molecular identification of resistance in plants uses a virus-induced gene silencing approach and can be used as an alternative transgenic approach for disease resistance. Using this method, Meyer et al. (2009) discovered the P. pachyrhizi-resistant accession PI459025B in soybean. Additionally, Pedley et al. (2018) employed this method to characterize Rpp1 in a recent study. According to this study, Rpp1 was situated on chromosome 18 between the flanking markers Sct 187 and Sat 064. According to results, the Rpp1 gene was found to be distinct among other Rpp genes as it provides an immune response to isolates of avirulent P. pachyrhizi and is known to produce ULP1-NBSLRR protein which is essential for the immunological response.

13.15.2 Gene Pyramiding

There are reports on the use of gene pyramiding in soybean to create resistance to soybean rust. Combining Rpp2, Rpp4, and Rpp5 in one soybean genotype demonstrated greater resistance to SBR (Lemos et al. 2011). Similarly, Rpp2, Rpp3, and Rpp4 were combined with cumulative resistance using the gene pyramiding strategy (Pedley et al. 2018). The gene pyramiding strategy to promote disease resistance in the soybean crop is clearly reflected in these results (Chander et al. 2019). Recently, it has been discovered that using marker-assisted selection in conjunction with line breeding can help create soybean cultivars that have ASR resistance genes. It contributed to the introduction of two new soybean varieties in Paraguay, namely, JFNC 1 and JFNC 2. Three all-stage resistance (ASR) genes, Rpp2, Rpp4, and Rpp5, were present in both cultivars (Kato et al. 2022).

13.15.3 Transcriptomics

RNA-seq analysis identified 52 differentially expressed genes (DEGs) DEGs, demonstrating soybean downy mildew (SDM) defence-responsive genes (Dong et al. 2018). These discoveries have opened the door for additional functional evaluation of potential candidate genes, which can then be exploited to create superior soybean cultivars with improved SDM resistance.

The differential expression of WRKY transcription factors (TFs) in SDM-high resistant (HR) and SDM-high susceptible (HS) genotypes was examined in order to provide new insights regarding the defence mechanism of soybean response to Pm infection. In addition, a total of 16 WRKY TFs were discovered to be specific in response to fungal inoculation, and 22 WRKY TFs were shown to be differentially expressed in HR and HS genotypes. The yeast one-hybrid (Y1H) experiment was used to test the capacity of the GmWRKY31 to bind the cis-acting W-box element in the promoter region of the GmSAGT1 gene, whose higher transcriptional expression was associated with increased SDM resistance (Dong et al. 2018).

13.16 Conclusion and Future Perspectives

Throughout this content, it has been discussed how fungal diseases affect soybean production globally and how much yield is lost as a result. Diseases have been consistently documented to cause significant yearly output losses in the millions of dollars in the literature for decades (Savary et al. 2019; Bandara et al. 2020). The most efficient and long-lasting method for managing disease in soybeans worldwide is genetic resistance, which serves as a crucial tenet supporting the global soybean value chain and food security. Since the discovery and use of molecular markers are intimately related to resistance genes, public and private soybean breeding programmes have consistently introduced vertical resistance through MAS. Despite the fact that our evaluation identified hundreds of key genomic areas that confer resistance to numerous fungal diseases, there are still other aspects of genetic resistance that need to be clarified and actively researched.

The development of high-density molecular markers based on next-generation sequencing (NGS) was made possible by advances in genomics. These markers quickly advanced and were affordable for use in both public and private breeding programmes (Song et al. 2013, 2020). The soybean genome has many novel regions that are significantly associated with resistance to various pathogens, according to genome-wide studies. Traits that were previously thought to be qualitative in nature have somewhat changed into quantitative traits, with major and minor alleles having small effects contributing to the observed phenotypes.

However, a successful genetic transformation mechanism is necessary for the generation of CRISPR/Cas9 transformants, though. Unfortunately, soybeans are a difficult commodity for plant transformation technology, and the majority of GE research are still in the early stages of development. Although a few studies have successfully demonstrated the introduction of ribonucleoprotein complex (Cas12a-RNP) in soybean protoplast (Kim et al. 2017), significant efforts may be required to incorporate these tools into soybean.