Among the major insect pests, BPH is one of the most destructive pests, especially in Asian countries including both tropical and temperate zones, causing severe economic loss to the rice crop through directly sucking phloem sap, often causing “hopper burn”, and it serves as a vector for transmission of rice ragged stunt virus (RRSV) and rice grassy stunt virus (RGSV) (Cabauatan et al., 2009). To date, more than 45 genetic loci providing BPH resistance have been identified from diverse plant materials, including cultivars, landraces, and wild rice species. Among them, seven genes (seven independent loci) comprising 10 different alleles for BPH resistance were cloned, that is, BPH14, BPH30, BPH17, BPH6, BPH29, BPH32=BPH3, and BPH1=BPH10=BPH18=BPH21/BPH2=BPH26/BHP7/BPH9. The cloned genes with physical locations, RAPDB/MSU gene ID, protein encoded, donor sources, and corresponding references are summarized in Table 1 . BPH14 gene encoding nucleotide-binding site (NBS) and leucine-rich repeats (LRRs), “NBS-LRR” or “NLR” in short, was first cloned from the previously mapped Qbp1 on Chr 3 of the Oryza officinalis introgression by genetic mapping and following transgenic complementation test (Du et al., 2009). With similar approaches, the BPH17 QTL on Chr 4S of the Sri Lankan rice variety, Rathu Heenati (Sun et al., 2005), revealed that three repeats of lectin receptor kinase gene (OsLecRK1-OsLecRK3) are responsible for BPH resistance (Liu et al., 2015). However, Liu et al. (2015) named the gene identified from the BPH17 QTL as BPH3 gene, and thus, it might cause confusion with the original BPH3 QTL mapped on Chr 6S of donors (PTB33 and Rathu Heenati varieties) (Jairin et al., 2007). To avoid confusion, we followed the original BPH17 QTL name as BPH17 gene name in this review. Afterward, Ren et al. (2016) cloned the causal gene of BPH resistance from the previously fine-mapped BPH3 locus of PTB33 (Jairin et al., 2007) using bioinformatics and transgenic validation experiments. The cloned gene encodes an unknown short consensus repeat (SCR) domain-containing protein and the BPH3 QTL was renamed as BPH32 (BPH32=BPH3) (Ren et al., 2016). Some of the BPH-resistant loci from different sources overlapped at the same locus, resulting in four clusters on chromosomes 4S, 4L, 6S, and 12L (Fujita et al., 2013; Du et al., 2020). From the largest BPH QTL cluster on Chr 12L containing BPH1, BPH2, BPH7, BPH9, BPH10, BPH18, BPH21, and BPH26 (Fujita et al., 2013), BPH26 encoding NBS-LRR protein was first cloned from the BPH26 QTL derived from ADR52 (Tamura et al., 2014). Then, BPH18 from the BPH18 QTL originated from the Oryza australiensis introgression line (IL) (IR65482-7-216-1-2) was cloned and identified as the same gene with BPH26 because physically two genes are located at the same locus on Chr 12L. However, the sequences, including promoter and protein-coding sequences (CDS) and also BPH reactions, were different between BPH26 and BPH18 (Ji et al., 2016). BPH9 derived from Pokkali was also identified as the same gene as BPH18/BPH26, but it showed different gene sequences and also different BPH reactions (Zhao et al., 2016), suggesting that all three are the same gene (locus) but functionally different alleles. Based on the sequence analysis of the Chr 12L BPH cluster, Zhao et al. (2016) classified the eight genes into four allelotypes, BPH1=BPH10=BPH18=BPH21/BPH2=BPH26/BHP7/BPH9. However, the BPH near-isogenic lines (NILs) with the same allele types (BPH10, BPH18, and BPH21) showed slightly different BPH resistance among the same allele types (Jena et al., 2017). Although four different functional alleles were identified on Chr 12L, they cannot be pyramided by MAS breeding due to their same locations. Guo et al. (2018) cloned the BPH6 encoding NBS-LRR protein from the previously found BPH6 QTL originating from the Swarnalata variety, which exhibits resistance to biotype 4, the most devastating BPH biotype in South Asia, of Bangladesh BPH populations (Kabish and Khush, 1988). The recessive gene BPH29 located at Chr 6 was found to encode a B3-domain containing protein from the RBPH54 IL possessing BPH resistance derived from the wild rice species Oryza rufipogon (Wang Y, et al., 2015). BPH30 gene located on Chr 4 of the indica variety AC-1613 was identified as a gene that encodes a novel protein with two leucine-rich domains (Shi et al., 2021). In addition to the cloned BPH genes, a number of QTLs and fine-mapped QTLs are also available (Fujita et al., 2013; Naik et al., 2018; Du et al., 2020). Moreover, using 10 different BPH genes/QTLs, 25 NILs possessing single or two to three genes were developed in an indica variety background, IR24 (Jena et al., 2017). The set of BPH NILs will be useful for screening suitable BPH genes/alleles against regional BPH biotypes and for genetic improvement of BPH resistance in the local elite variety backgrounds. To achieve durable and broad-spectrum resistance, QTL/gene pyramiding approaches are widely used in breeding programs. Overall, the BPH-NILs with two to three genes exhibited more strong and broad-spectrum resistance than the NILs harboring a single BPH gene (Jena et al., 2017). In addition, pyramiding effects of two to three BPH gene combinations such as BPH14 + BPH15, BPH6 + BPH12, and BPH13 + BPH14 + BPH15 were observed in different backgrounds or breeding programs (Hu et al., 2012; Qiu et al., 2012; Hu et al., 2016).

A handful of genetic factors governing resistance against planthoppers, including small brown planthopper (SBPH: Laodelphax striatellus), white-backed planthopper (WBPH: Sogatella furcifera), green leafhopper (GLH: Nephotettix virescens), and green rice leafhopper (GRH: Nephotettix cincticeps), have been identified from diverse germplasms and are well summarized in a few review papers (Fujita et al., 2013; Du et al., 2020). In this review, we only included recent progress on genetic factors to other planthoppers. A stable locus showing WBPH resistance in 2 years was found in the RM280-RM6909 region on Chr 4L from the Cheongcheong variety (Kim et al., 2021). The high resistance locus designated as Bph38 to both BPH and WBPH was identified from O. rufipogon and was fine-mapped to a 79-kb region on Chr 4 (Yang et al., 2020). Phi et al. (2019) identified a major QTL (qGRH4.2=GRH6) conferring GRH resistance from a wild species (Oryza nivara_IRGC105715) and fine-mapped the locus to ~31-kb region on Chr 4. Recent studies showed a possibility that increasing resistance to multiple insects could be achieved by the pyramiding of insect resistance loci. For example, both GLH and GRH resistance was obtained by pyramiding of two GRH resistance genes, GRH2 and GRH4 (Horgan et al., 2018); enhanced resistance against multiple herbivore species, including zig-zag leafhopper (Recilia dorsalis), BPH, and WBPH, was shown by pyramiding of two to three GRH resistance loci (GRH2 and GRH4-6) (Horgan et al., 2019).

To date, 12 potential genetic factors (Gm1–Gm12) conferring resistance against Asian rice gall midges (O. oryzae) have been reported. Among them, 10, except for Gm9 and Gm10, are mapped on rice chromosomes (Bentur et al., 2016; Leelagud et al., 2020). Although no Gm genes have been fully validated by using transgenic approaches, four QTLs were fine-mapped with potential candidate genes: gm3 (donor: RP2068-18-3-5 breeding line from Velluthacheera) on 560-kb region of Chr4L (Sama et al., 2014), Gm4 (donor: Abhaya) on 300-kb region of Chr 8 (Divya et al., 2015), Gm8 (donor: Aganni) on 430-kb region of Chr 8 (Divya et al., 2018), and gm12 (donor: MN62M) on 345-kb region of Chr 2 (Leelagud et al., 2020). These four QTLs might be useful in a breeding program. However, the donor sources showing resistance against Indian gall midge biotypes, including Velluthacheera (gm3), Abhaya (Gm4), and Aganni (Gm8), were susceptible to all eight Thailand gall midge populations (Leelagud et al., 2020), suggesting that the suitable genetic factors should be selected based on the potential biotypes of insects.

Five QTLs associated with leaf-folder (Cnaphalocrocis medinalis) resistance, with 8.0%–21.1% phenotypic variance explained (PVE), were found from the double haploid population (CJ06 × TN1), and pyramiding of QTLs affected resistance to leaf-folder (Rao et al., 2010). However, reliable genetic factors controlling other insect resistance, including stem borer and grain-sucking bugs, have not been reported yet.

Among the fungal diseases, rice blast is the most devastating fungal disease of rice worldwide, causing a serious threat to the world’s food security. The blast pathogen can affect all above-ground parts of a rice plant, including the leaf, collar, node, neck, parts of the panicle, and sometimes the leaf sheath (IRRI Rice Knowledge Bank). Blast disease occurs in 85 countries, and it causes a 10%–35% loss of harvest (Fisher et al., 2012), and the amount of rice damaged by blast annually is sufficient to feed 60 million people worldwide (Pennisi, 2010; Fahad et al., 2019; Singh et al., 2020). There are over 100 blast resistance QTLs/loci identified from diverse germplasm including cultivars, landraces, and wild relatives of rice (Ashkani et al., 2016; Li et al., 2019). The Pib (donor: indica cultivar Engkatek) and Pita (donor: indica cultivar Tadukan) were the first cloned blast resistance genes, and both encode NBS-LRR domains predicted to be cytoplasmic proteins (Wang et al., 1999; Bryan et al., 2000). To date, 23 genes (23 independent loci) consisting of ~35 different alleles have been cloned, including three panicle blast resistance genes Pb1–Pb3 ( Table 2 ). The cloned genes were distributed across the rice chromosomes except for chromosomes 5, 7, and 10. Chromosomes 6 and 11 harbored four and six blast genes, respectively (Pi9 alleles, Pid4, Pid3 alleles, and Pid2 on Chr 6; Pia alleles, Pi54rh alleles, Pik alleles, Pb1, Pb2, and Pb3 on Chr 11). Several blast-resistant QTLs were identified at the same location on the short arm of Chr 6 (10.4-Mb region) from different germplasms. Finally, the causal genes were located at the NLR gene-repeated cluster (Pi9 locus), and they are regarded as the same genes with different alleles (Pi9/Pi2=Piz-5/Piz-t/Pi50/Pigm/Pizh). At the Pi9 locus, two to 13 repeats of NLR gene were laid next to each other, and the blast-resistant donors possessed nine repeats (Pi9 and Pi2) or 13 repeats (Pigm) of NLR genes (Deng et al., 2017). There were sequence variations among the alleles of the responsive NLR gene at the Pi9 locus, and they showed different reactions to the blast strains. In addition to the cloned genes/alleles, one major QTL (Pi40) was identified at the Pi9 locus from the O. australiensis-derived IL (IR65482-4-136-2-2) through fine mapping (Jeung et al., 2007). The Pi40 introgression in Korean and Turkish varieties showed resistance to a wide range of blast strains in Korea and Turkey (Jeung et al., 2007; Beser et al., 2016). Another major cluster was found on Chr 11 (25.2-Mb region) (Pik locus) from various donor materials, and they (Pik/Pik-m/Pik-p/Pi1/Pi7) were identified as allelic ( Table 2 ). Interestingly, most of the cloned blast genes encode NBS-LRR (NLR) protein, except for four genes: bsr-d1 (C2H2-type zinc finger protein), pi21 (proline-rich protein), Pid2 (B-lectin receptor kinase), and Ptr=Pita2 (armadillo repeat protein). The majority of blast-resistant donor alleles/genes are dominant except for pi21, which is recessive (Liu W, et al., 2013). Pi21 encodes a proline-rich protein, and the loss-of-function allele from the resistant donor (Owarihatamochi) confers non-race-specific resistance. pi21 gene was closely linked to the gene providing poor eating quality. However, the genes were successfully separated by recombination between two genes in the breeding lines, and blast resistance with good eating quality was achieved (Fukuoka et al., 2009). Thus, precise introgression with the cloned target genes is able to reduce the presence of unwanted phenotypes in the final breeding products caused by “linkage drag”. Among the cloned blast genes, Pi50, Pizh, Pi54rh, Pi56, Pi64, PigmR, and Ptr=Pita2 alleles were known as broad-spectrum resistance (Liu et al., 2021). A few sets of NILs with blast resistance sources were developed in both japonica and indica backgrounds: 20 NILs with 11 blast QTLs/genes in japonica background Lijiangxintuanheigu (LTH) (Telebanco-Yanoria et al., 2010) and 28 NILs with 14 QTLs/genes in an indica background, CO39 (Telebanco-Yanoria et al., 2011). Moreover, both NIL sets were tested by 20 blast isolates collected in the Philippines. Recently, 21 NILs with 18 QTLs/genes in another indica background, US-2, were developed, and the NILs were tested with 31 isolates from Asia (Japan, China, the Philippines, Indonesia, Vietnam, Cambodia, Bangladesh, and Laos) and Africa (Nigeria, Kenya, and Benin) (Fukuta et al., 2022). In blast bioassay with the NIL sets above, most of the genes/QTLs showed differential reactions against different isolates, even in the same country collections, suggesting that the selection of suitable blast genes/alleles based on the local pathotypes/isolates is important to develop blast resistant varieties. Among the blast genes used in the NIL development above, NIL-Pi9 exhibited resistance or moderate resistance to all 31 isolates from Asia and Africa (Fukuta et al., 2022), suggesting that Pi9 allele might be useful to breed blast-resistant variety across the rice cultivation countries. The sets of NILs and blast screening data against various isolates will be very useful to pathology studies, the selection of suitable genes/alleles against regional isolates, and breeding programs. To achieve durable and broad-spectrum resistance, pyramiding of resistance genes (two or more) in one background is usually used in the breeding program. There are various gene combinations of blast genes that prove the enhanced blast resistance in both indica and japonica rice against several blast isolates. Two genes–pyramided lines with Pi37 + Pid3, Pi5 + Pi54, Pi54 +Pid3, and Pigm + Pi37 exhibited significantly enhanced resistance and observable additive effects (Jiang et al., 2019). The gene combinations Pigm + Pi1, Pigm + Pi54, and Pigm + Pi33 displayed broad-spectrum resistance (Wu et al., 2019). Broad-spectrum blast resistance was also achieved in the temperate japonica varieties by pyramiding three to four genes with Piz, Pib, Pik, Pita, and Pita2 (Zampieri et al., 2023). As proven in many previous studies, stacking suitable blast genes/alleles has strong potential to obtain durable and broad-spectrum resistance in the breeding program.

In contrast to leaf blast resistance, genetic resources for blast disease on other organs/tissues are relatively poor. The first panicle blast resistance gene, Pb1, encoding NBS-LRR was cloned from an indica cultivar Modan (Hayashi N, et al., 2010). Afterward, it was found that panicle blast resistance by Pb1 is dependent on at least four other loci (Inoue et al., 2017), suggesting that a level of panicle blast resistance with Pb1 will be influenced by other genetic factors or background materials. Recently, two additional panicle blast resistance genes, Pb2 and Pb3, were identified through GWAS and validated by transgenic approaches (Ma et al., 2022; Yu et al., 2022). Both genes encode NBS-LRR proteins and are physically close to each other (~360-kb distance between Pb2 and Pb3). Some of the cloned leaf blast genes, such as Pi25 (Chen J, et al., 2011), PigmR (Deng et al., 2017), and Pid4 (Chen et al., 2018), also showed some level of panicle blast resistance.

To identify the genetic factors governing bakanae disease resistance, QTL mapping and GWAS have been conducted and identified a handful of QTLs on chromosomes 1, 3, 4, 9, and 10 from several different donors, but no genes have been cloned yet. Three major QTLs (qBK1, qBK1.1, and qFfR1) were fine-mapped on the Chr 1 region between 23.32 and 23.67 Mb (Lee et al., 2021).

A number of QTLs for false smut resistance have been identified by QTL mapping with bi-parental populations (Andargie et al., 2018; Han et al., 2020; Neelam et al., 2022) and GWAS (Hiremath et al., 2021). The results suggested that false smut resistance seems to quantitate traits governed by multiple genes. Among the QTLs, qFsr8–1 originated from the Chinese rice landrace MR183–2 and showed the highest PVE (26.0%).

More than 200 QTLs associated with sheath blight (ShB) resistance have been identified from the diverse mapping populations (Zarbafi and Ham, 2019; Goad et al., 2020). Among all the identified ShB QTLs, two loci on Chr 9 (qShB9-2) and Chr 11 (qSBR11-1) contribute 25% and 14% of PVE, respectively, are the major effect QTLs (Molla et al., 2020), and may be useful in a breeding program.

For brown spot (BS) resistance, susceptible and resistant germplasms were identified by several studies. Several cultivars that have been categorized as resistant did not show complete resistance (immunity), but they showed quantitative resistance to BS. To date, more than 20 QTLs with low–mild phenotypic variation (<20%) were identified from several mapping populations, including recombinant inbred lines (RILs), doubled haploid lines (DHLs), and chromosome segment substitution lines (CSSLs) from several different donors (reviewed by Mizobuchi et al., 2016). One major QTL, qBSR11-kc, showing 23.0%–25.9% of the total phenotypic variation was identified from indica variety CH45 (Matsumoto et al., 2017).

The genetic architecture of narrow brown spot (narrow brown leaf spot) resistance was almost unknown. A recent genetic analysis using the RIL population derived from the cross between two US varieties (Cypress and LaGrue) identified a single large-effect QTL, CRSP-2.1, explaining 81.4% of the phenotypic variation (Addison et al., 2021). The causal gene is not confirmed yet, but the major QTL might be useful in a breeding program.

Aggregate sheath spot disease has been reported in many Asian countries, as well as the USA, South America, and Australia, and it can cause ~20% of yield loss (Lanoiselet et al., 2007). Good levels of resistance to aggregate sheath spot were identified from O. rufipogon and successfully transferred into cultivars (McKenzie et al., 1994). Recent GWAS with tropical japonica and indica populations identified a handful of QTLs (Rosas et al., 2018).

Rice sheath rot diseases are found in most rice-growing areas of the world and cause 20%–85% ranges of yield losses, making it an emerging ubiquitous destructive disease of rice (Bigirimana et al., 2015). However, rice sheath rot is less studied, and no reliable germplasm or genetic factors have been identified yet.

Stem rot disease resistance was found in wild rice species (O. nivara and O. rufipogon) and weedy rice (O. sativa f. spontanea) (Figoni et al., 1983), and the stem rot resistance was successfully transferred from O. rufipogon to California rice cultivars through interspecific hybridization (Oster, 1992). Recently, several QTLs for stem rot resistance were identified from indica germplasm through a GWAS analysis (Rosas et al., 2018).

Among the bacterial diseases, BB caused by Xoo is the most destructive bacterial disease in rice. Thus, it has been intensively studied for the isolation of BB-resistant germplasm, genetic analysis, gene identification, and molecular mechanism of wars between Xoo and rice. To date, at least 47 Xoo resistance QTLs and genes (named Xa genes) have been identified from diverse germplasms, including cultivated rice, rice mutant lines, and wild rice species. Xa21 from Oryza longistaminata introgression line (IRBB21) was first cloned in 1995 by Song et al. and followed by Xa1 from the IRBB1 line (Yoshimura et al., 1998). Later, Xa2, Xa31(t), CGS-Xo1, Xa14, and Xa45(t) were identified as a group of Xa1 allelic R genes (Ji et al., 2020). Currently, 13 different genes/loci consisting of ~23 allelotypes have been cloned and characterized ( Table 3 ), that is, Xa1/Xa2=Xa31(t)/Xa14/Xa45(t)/CGS-Xo1, Xa3=Xa26, Xa4, xa5, Xa7, Xa10, xa13/OsSWEET11/Os8N3, Xa21, Xa23, Xa47(t), xa25/OsSWEET13/OsMtN3, Xa27, and xa41(t)/OsSWEET14/Os11N3. The 13 cloned BB resistance genes encode several types of proteins: NBS-LRR (Xa1/Xa1 alleles and Xa47(t)), leucine-rich repeat receptor-like kinases (LRR-RLKs) (Xa3=Xa26 and Xa21), a cell wall-associated kinase (WAK) (Xa4), executor R proteins (Xa7, Xa10, Xa23, and Xa27), SWEET/sugar transporter proteins (xa13/OsSWEET11, xa25/OsSWEET13, and xa41(t)/OsSWEET14), and a transcription factor gamma subunit protein (xa5). The genes encoding NBS-LRR, LRR-RLK, and WAK are involved in pathogen recognition and activation of the innate immune system, whereas the genes encoding executor R proteins are transcriptionally activated by the Xoo transcription activator-like (TAL) effector protein and trigger programmed cell death (PCD)-based hypersensitive response (HR). Thus, for the genes mentioned above, the functional alleles from the BB-resistant donor sources are dominant. In contrast, BB resistance is caused by sequence mutations at the TAL effector binding sites in the promoter of the SWEET (Sugar Will Eventually be Exported Transporter) genes and thus a recessive allele. BB resistance of xa5 gene relies on one amino acid difference between resistance and susceptible lines in Xa5 protein (a general eukaryotic transcription factor), and the BB-resistant allele is recessive (Iyer and McCouch, 2004). The cloned 13 genes are distributed on six chromosomes (one gene each on Chr 4, 5, 8, and 12; two genes on Chr 6; six genes on Chr 11) ( Table 3 , Figure 1 ). Six cloned genes on Chr 11 are closely located to each other in ~10.2-Mb size (18.2–28.4-Mb region on Chr 11) ( Figure 1 ). Thus, in the case of gene pyramiding using the six genes on Chr 11, breeders need to consider producing enough progenies for obtaining pyramided alleles that occur by recombination between two closely located genes. Several cloned genes, including Xa7, Xa23, xa41, and Xa47, were reported as broad-spectrum resistance genes/alleles (Liu et al., 2021). NILs with single BB resistance genes were developed through IRRI-Japan collaboration designated as “IRBB” lines (Ogawa et al., 1991), and additional NILs (IRBB) with single or multiple BB resistance genes (two to five genes) were developed in the BB-susceptible background IR24 at IRRI, Philippines. Differential reactions of the NILs (IRBB lines) with single and pyramided Xa genes to 11 races in the Philippines were observed, and the results are available at the IRRI Rice knowledge bank (http://www.knowledgebank.irri.org/ricebreedingcourse/Breeding_for_disease_resistance_Blight.htm). The IRBB lines possessing multiple Xa genes (two to five genes) exhibited broad-spectrum resistance than the single gene introgression IRBB lines. Similarly, pyramiding of Xa genes such as Xa21 + Xa33, Xa21 + xa13 + xa5, and Xa4 + xa5 + Xa7 + xa13 + Xa21 offers greater and broader resistance to Xoo than an individual resistance gene (Pradhan et al., 2015; BalachIranjeevi et al., 2018; Hsu et al., 2020). The IRBB sets were also tested with 16 isolates in Korea, and the results showed that xa5 was strong and broad-spectrum resistant than any other Xa genes (Jeung et al., 2006). Rice possessing Xa7 exhibited less disease than lines without Xa7 over 11 years in the Philippines, even though the virulence of Xoo field populations increased. In addition, Xa7 restricted disease more effectively at high temperatures, while other Xa genes were less effective at high temperatures (Webb et al., 2010). The IRBB lines and stacked information including gene reactions, spectrum, durability, and influence of environments will be useful to select suitable genes/alleles for regional/local breeding programs and also for the development of durable and broad-spectrum resistant rice varieties.

For BLS resistance, a handful of QTLs with low-to-moderate PVEs (2.64%–15.93%) were identified (Tang et al., 2000). In addition, a recent GWAS using 510 diverse rice accessions identified 79 quantitative trait nucleotides (QTNs) reflecting 69 QTLs for BLS resistance (Xie et al., 2021). However, no BLS resistance gene has been cloned yet. Among the BLS-resistant QTLs, the highest effect QTL, qBlsr5a (12.84%–15.93% PVE), was fine-mapped to 30.0-kb interval on Chr 5, and the resistant parent allele of Os05g01710 gene within the fine-mapped region was identical to xa5, which is one of major BB resistance genes, suggesting that Os05g01710 (xa5) is possibly the candidate gene of qBlsr5a (Xie et al., 2014).

“Rice sheath rot” disease symptoms can be caused by the bacterial pathogen “P. fuscovaginae” and also by the fungal pathogen “S. oryzae”. A recent pathobiomes study revealed that P. fuscovaginae and S. oryzae were prevalent in symptomatic rice samples in highland and lowland, respectively, in Burundi, indicating that the pathogens exist independently and are not part of a complex disease (Musonerimana et al., 2020). However, no reliable resistant germplasm and genetic factors have been identified yet.

Bacterial panicle blight (BPB), BSR, and BGR are caused by the same bacterial pathogen, B. glumae. It was first reported as BGR in Japan in 1955. Since then, BPB has been found in more than 18 countries globally including Asia, Africa, and North and South America (Zhou, 2019; Ortega and Rojas, 2021). Although it is an emerging disease globally, only several cultivars with partial resistance and 12 QTLs associated with partial resistance have been reported (Zhou, 2019). Regarding BSR resistance, one QTL (RBG1/qRBS1) was identified from the CSSL population (Nona Bokra introgressions in Koshihikari background) (Mizobuchi et al., 2016). For BGR resistance, 13 QTLs have been found from the two mapping populations: a BIL from Kele (R) × Hitomebore (S) and a RIL from TeQing (R) × Lemont (S) (Mizobuchi et al., 2016).

Rice tungro disease is a serious threat to rice production in South and Southeast Asia. Tungro disease viruses are transmitted from tungro-infected plant to another by leafhoppers. The most efficient vector is the green leafhopper (IRRI Rice Knowledge Bank). Tungro was found to be associated with two distinct viruses: RTSV and RTBV. A series of large-scale outbreaks of tungro were recorded in India, Thailand, Indonesia, Malaysia, the Philippines, Thailand, China, and Bangladesh. Tungro, as one of the destructive diseases of rice, causes yield losses of 5% to 10% annually and is estimated to cause an annual loss in rice production of approximately 1.5 billion US dollars worldwide (Dai and Beachy, 2009). In the late 1990s, several tungro-resistant sources, including landrace and wild species, were isolated and used in the breeding program by IRRI, and the most promising breeding lines were developed by crossing with Utri Merah donor (Azzam and Chancellor, 2002). Afterward, Encabo et al. (2009) revealed that RTBV and RTSV are inherited separately from rice accession Utri Merah, conferring resistance to both RTBV and RTSV, and Lee et al. (2010) cloned the causal recessive gene (named as tsv1) involved in RTSV resistance in Utri Merah. TSV1 encodes eukaryotic translation initiation factor 4G (eIF4G), and mutation on the protein-coding sequence of TSV1 in Utri Merah (tsv1 allele) may impair the RTSV RNA translation, resulting in tungro resistance. The tsv1-Utri Merah allele is widely used for tungro resistance improvement in many breeding programs.

Since RYMV was first discovered in Kenya in 1970, it has been reported from only the countries in the African continent. RYMV causes the most serious damage in Africa among all the rice diseases. Primary infection of RYMV in rice fields is mediated by beetle family chrysomelids, and secondary spread occurs mainly through mechanical contact between infected and healthy leaves by wind (Kouassi et al., 2005). In the past, farmers have been advised to use chemicals to eliminate beetle vectors. The most effective and sustainable way to manage RYMV is to use tolerant and resistant varieties (Abo et al., 1997).

High RYMV resistance was found in one African rice cultivar (Oryza glaberrima), Tog5681, and one O. sativa cultivar, Gigante. Evaluation of the crosses of these two highly RYMV-resistant cultivars suggests the presence of a single recessive gene (Ndjiondjop et al., 1999). Later, it was discovered that the gene is RYMV1, and the gene encodes a eukaryotic translation initiation factor, eIF4(iso)4G (Albar et al., 2006). In sequence comparisons with the dominant susceptible allele (Rymv1-1), four different recessive resistant alleles from one O. sativa var. Gigante (rymv1-2) and three O. glaberrima accessions (Tog5681 (rymv1-3), Tog5672 (rymv1-4), and Tog5674 (rymv1-5)) were characterized by the presence of short amino acid substitutions or short deletions in the MIF4G domain of the protein (Albar et al., 2006; Thiémélé et al., 2010). Allele-specific markers targeting mutations or deletions characterizing different RYMV1 were developed for improving MAS for the introduction of the resistance alleles into susceptible cultivars of O. sativa or O. glaberrima (Thiémélé et al., 2010). In the second major recessive resistance gene, RYMV2, it was identified that 1-bp deletion on the coding sequence of the rice homolog of the Arabidopsis CPR5 gene, known to be a defense mechanism regulator, from the resistant African rice (O. glaberrima) Tog7291 provided RYMV resistance (Orjuela et al., 2013). A single dominant resistant gene RYMV3 encoding NBS-LRR protein was identified from the O. glaberrima Tog5307 (Pidon et al., 2017). Novel resistant alleles and accessions for RYMV2 and RYMV3 were identified by screening 268 O. glaberrima accessions and sequencing (Pidon et al., 2020), and five new resistant germplasm were isolated from Korean rice lines (Asante et al., 2020). The cloned genes with different resistant alleles will be useful to improve RYMV resistance, especially for the breeding program for the African continent.

RSV is an RNA-type virus belonging to the genus Tenuivirus, and it is transmitted by SBPHs. RSV has been reported only in China, Japan, Korea, and Taiwan, where japonica rice is cultivated, and it caused severe damage to the rice fields in Eastern China, Japan, and Korea. While most indica varieties are resistant to RSV, the majority of japonica varieties are highly susceptible. A number of RSV-resistant QTLs have been reported from diverse indica-resistant donors, and the major QTLs were repeatedly detected on Chr 11 among several QTL mapping (Cho et al., 2013). Finally, the major QTL, qSTV11, originated from an indica variety Kasalath and was cloned (Wang et al., 2014). STV11-Kasalath allele encodes a sulfotransferase (OsSOT1) protein catalyzing the conversion of salicylic acid (SA) into sulfonated SA (SSA), whereas the protein encoded by the susceptible allele STV11 loses this activity. STV11 gene will be useful in improving RSV resistance in the japonica varieties.