Targeted genome editing technology such as CRISPR/Cas9 can be used efficiently to develop disease-resistant bananas. The accessibility of full banana genome-sequences and the CRISPR/Cas9 gene-editing systems has made it easy to generate disease-resistant banana by precisely knocking out the endogenous genes (Ntui et al., 2020). Several susceptibility genes associated with bacterial resistance have been identified and targeted for editing in several plants (Tripathi et al., 2020).

Researchers at the International Institute of Tropical Agriculture (IITA) are developing banana resistant to BXW disease. All the cultivated varieties are susceptible to BXW disease. There is no known source of resistance against the bacterial pathogen within Musa germplasm except for the wild-type diploid banana progenitor “Musa balbisiana” (Tripathi et al., 2019a). The knowledge of resistance mechanisms in wild-type banana against a bacterial pathogen can be utilized for developing resistant varieties through the editing of genes related to susceptibility and/or negative regulation of plant immunity or activating the defense genes. To identify the Musa genes for developing the BXW-resistant varieties, we investigated the molecular basis of disease resistance in banana progenitor Musa balbisiana. The comparative transcriptomic analysis of Musa balbisiana, a wild-type progenitor resistant to BXW, and the highly susceptible banana cultivar “Pisang Awak” inoculated with Xanthomonas campestris pv. musacearum, identified a couple of susceptibility genes, nutrient transporters, E3 ubiquitin-protein ligase, pathogen-associated molecular patterns, receptor kinases, antimicrobial peptides, resistance proteins, and defense signaling genes associated with BXW resistance (Tripathi et al., 2019a).

Another approach we are using is to transfer the knowledge on bacterial pathogen resistance from other plant species to the banana. We have demonstrated the knockout of Musa Downy mildew resistance 6 (Musa DMR6) gene in edited banana cultivar “Sukali Ndiizi” enhanced resistance to BXW disease (Tripathi et al., 2021). DMR6 encodes a 2-oxoglutarate Fe (II)-dependent oxygenase (2OGO) and was characterized as a negative regulator of plant defense by hydrolyzing the plant defense signaling molecule salicylic acid (Zhang et al., 2017). It is upregulated during pathogen infection (Low et al., 2020). We performed a phylogenetic analysis of the 2-oxoglutarate Fe(II)-dependent oxygenase gene family with five plant species, including Musa acuminata, Musa balbisiana, Arabidopsis thaliana, Solanum lycopersicum, and Nicotiana tabacum (Tripathi et al., 2021). AtDMR6 orthologues were identified in Musa spp., and one of the MusaDMR6 orthologue (Ma04_p20880.1) was selected for analysis as a putative candidate. Banana mutants were generated targeting the MusaDMR6 orthologue, and mutations were confirmed by sequencing. The Musadmr6 mutants generated by a multiplexed CRISPR/Cas9 construct were evaluated in the greenhouse for resistance to BXW disease. The edited events showed enhanced resistance to BXW, and no morphological abnormalities were observed (Tripathi et al., 2021).

Banana streak virus (BSV), a dsDNA virus belonging to badnaviruses, integrates into the host plant genome creating a significant challenge in banana breeding and germplasm movement. A CRISPR/Cas9 system was used to inactivate the integrated endogenous BSV (eBSV) by targeting all three open reading frames (ORF) of the virus (Tripathi et al., 2019). The regenerated genome-edited plants of “Gonja Manjaya” showed targeted mutations in the integrated eBSV sequences in the host genome. As the eBSV gets activated into infectious viral particles under stress conditions leading to the development of disease symptoms, the genome-edited plants were water stressed in the greenhouse. Most of the mutants remained asymptomatic compared to the control non-edited plants under water stress conditions, confirming the silencing of the reactivation of eBSV into infectious viral episomal proteins.

Several banana researchers are developing banana varieties resistant to fusarium wilt disease. In the 1950s, Fusarium wilt race 1 outbreak wiped an entire “Gros Michel” farm and was replaced by “Cavendish” varieties, which currently cover about 90% of export markets (Ploetz, 2015). Management of diseases has mostly been achieved using chemical and resistant cultivars (Tripathi et al., 2019b). However, the evolution of new ecotypes makes using new breeding tools such as genome editing to generate resistance a continuous requirement. As of now, no work has been published on the use of genome editing in a banana for resistance to fungal pathogens. However, editing of susceptibility genes such as Mildew resistance locus O (MLO), LATERAL ORGAN BOUNDARIES (CsLOB1), DMR6, ERF922, amongst others, have been shown to confer resistance to fungal diseases (Jia et al., 2016; Wang et al., 2016; Peng et al., 2017; de Toledo Thomazella et al., 2021; Li et al., 2022). These approaches can be adopted in banana to generate resistance against fusarium wilt and black Sigatoka. Currently, researchers at IITA are testing the edited banana with S gene knockout in the greenhouse for resistance against fusarium wilt disease.

Biofortification is a cost-effective approach to increase vitamins and minerals in food crops and ameliorate malnutrition (hidden hunger). Vitamin A deficiency, one of the most dominant micronutrient deficiencies, affects people in Africa. Genome editing has significant potential to enhance micronutrient bioavailability in crops through biofortification.

Some progress has been reported in enhancing nutrients such as iron, zinc, carotenoid, and amino acids in different crops like camelina, grape, potato, rapeseed, rice, sweet potato, tomato, and wheat using CRISPR/Cas9 technology targeting various genes (Liu et al., 2021). Recently, Kaur et al. (2020) applied CRISPR/Cas9 technology to increase β-carotene content in the Cavendish cultivar “Grand Naine” by editing the lycopene epsilon-cyclase (LCYε) gene. They showed that the edited lines had enhanced accumulation of β-carotene content up to 6-fold (∼24 μg/g) in the fruit pulp compared to the unedited plants. The editing of genes regulating zinc, iron, amino acids, and other nutrients could also be targeted in banana to increase the nutrient contents.

Most of the cultivated banana varieties are very tall, and some of them are challenged by the weak lodging and severely damaged during storms. Dwarf and semi-dwarf varieties are better for crop growth and harvesting. Therefore, researchers are trying to develop semi-dwarf and dwarf banana varieties. Gibberellin (GA) is a critical gene determining plant height and mutations in its biosynthesis genes usually produce dwarf phenotypes. Shao et al. (2020) demonstrated that CRISPR/Cas9 tool could be applied to develop semi-dwarf plants by editing the Musa acuminata gibberellin 20ox2 (MaGA20ox2) gene, disrupting the GA pathway in banana cultivar “Gros Michel.”

Banana is a climacteric fruit with a soft texture upon ripening. Generally, banana ripens fast and start decaying within a week. The delay in the ripening of banana fruit can enhance its limits on storage, transportation, and marketing and reduce postharvest losses. CRISPR/Cas9-mediated genome editing of banana targeting the aminocyclopropnae-1-carboxylase oxidase (MaACO1) demonstrated delayed ripening, enhancing the shelf life of fruit (Hu et al., 2021). The edited banana fruits showed reduced ethylene synthesis and extended shelf life under natural ripening conditions.

Development of resistance to the two major devastating viral diseases of cassava, CMD and CBSD, has been attempted using CRISPR/Cas9 technology (Gomez et al., 2019; Mehta et al., 2019). To generate plants with resistance to CMD, Mehta et al. (2019) targeted the viral AC2 gene coding for the multifunctional TrAP protein involved in gene activation, virus pathogenicity, and suppression of gene silencing, and the AC3 gene coding for the REn protein involved in replication enhancement using single gRNA. In this study, the transgenic cassava lines expressing Cas9 gene along with a gRNA targeting the viral genome did not show resistance to CMD under greenhouse conditions. The authors further sequenced full-length viral amplicons from the infected transgenic and wild type plants. Different types of mutations in the viral genome were observed, including deletions within the gRNA target site that resulted in premature stop codon within the AC2 and AC3 ORFs. The indels were observed in viruses infecting all plants, including control wild-type plants. One major observation from this study was the introduction of histidine (H) to glutamine (Q) amino acid in the AC2 ORF of the viruses infecting the transgenic cassava plants. This H to Q mutation was a result of a single nucleotide (“T”) insertion that rendered the gRNA target impossible to bind and cleave. The authors observed about 33–48% of edited virus genomes evolve a conserved single nucleotide mutation in AC2 that confers resistance to CRISPR/Cas9 cleavage. The authors concluded that the CRISPR/Cas9 system may not be effective for developing resistance against Geminivirus as it may lead to virus evolution. However, this generalization has since been rebutted (Rybicki, 2019). The major argument in the rebuttal by Rybicki (2019) is that the mutation could have arisen spontaneously even in the wild-type virus rather than it being selected by CRISPR/Cas9 as detailed in Mehta et al. (2019). Rybicki (2019) further argues that resistance to other begomoviruses has been successfully demonstrated in other plants without resulting in Mehta’s observations (Baltes et al., 2015). The other major limitation of the Mehta et al. (2019) study is using only one gRNA that targeted one viral region (AC2). It would be ideal to experimentally target other viral ORFs and check if similar trends in virus evolution are observed.

The use of CRISPR/Cas9 to generate cassava resistant to the CBSD, the second major cassava virus, has also been attempted (Gomez et al., 2019). In this study, they used the fact that viruses in the potyviridae family use the eukaryotic translation initiation factor 4E (eIF4E) and novel cap-binding protein (nCBPs) to initiate cap-dependent messenger RNA translation. A CRISPR/Cas9 system targeting nCBPs was developed to introduce mutations that attenuated CBSD aerial symptoms in the mutants. This study only targeted the two nCPBs in cassava and multiplexing to target the other three eIF4Es could be done to achieve increased resistance.

The plant bacterial pathogens of the genus Xanthomonas promote pathogenicity by injecting effector proteins through the type III secretion system. Some of the injected proteins are transcriptional activator-like effectors (TALE), which control transcription in a manner similar to eukaryotic transcription factors (TFs) (Cox et al., 2017). The TALEs bind at specific promoter regions in the susceptibility genes called effector-binding elements (EBEs). These susceptibility genes are involved in sugar transport (SWEET genes), and their expression possibly provides energy source for the bacteria. Modification of Xanthomonas EBEs through genome editing has been observed to result in disease resistance (Xu et al., 2019; Li et al., 2020; Zafar et al., 2020). Similar efforts could be applied in cassava where promoters of susceptibility genes can be identified and modified to generate resistance lines. A recent report details efforts to develop CBB resistance through CRISPR/Cas9-based editing of the promoter of the cassava MeSWEET10a gene (Wang et al., 2022). The cassava mutants conferred enhanced resistance to CBB disease. The events also showed normal morphological and yield-related traits similar to the wild type.

Conventional breeding in cassava is time-intensive, taking a minimum of 6 years to get to cultivar trials and even longer to release a cultivar. The breeding time is lengthened by variation in plant performance on the physiological status of the vegetative cutting and mostly by delayed and non-synchronized flowering of cassava breeding lines (Adeyemo et al., 2019). Approaches that can shorten the flowering time and synchronize flowering will go a long way in enhancing breeding and cultivar improvement in cassava (Ceballos et al., 2015).

Targeting flowering-related genes using CRISPR/Cas9 is a plausible approach that can be used to induce flowering in cassava. Silencing of flowering repressor using CRISPR/Cas9 has resulted in early flowering mutants in soybean (Han et al., 2019). In this study, CRISPR/Cas9 targeted a soybean flowering repressor gene E1, resulting in early flowering. The edited soybean line showed photoperiod insensitive flowering, allowing it to grow at different altitudes. Cassava, just like soybean, is a long-day crop and is dependent on extended photoperiod to flower. Mapping the major genes involved in photoperiod-dependent flowering in cassava could facilitate a study like Han et al. (2019) to develop photoperiod-insensitive cassava lines. Early flowering through CRISPR/Cas9 has also been achieved in Chinese cabbage (Jeong et al., 2019). This study used six gRNAs to target the Flowering locus C (FLC) in Chinese cabbage. The knockout obtained had early flowering as well as vernalization-independent phenotypes. Cassava has multiple FLC locus that needs to be experimentally characterized. The CRISPR/Cas9 editing approach by Jeong et al. (2019) is applicable in cassava for first functionally characterizing the FLC and target FLC versions involved in repressing flowering.

Induction of flowering through an inducible CRISPR/Cas9 system is a better option compared to constitutive overexpression. Inducible CRISPR/Cas9 systems are still under development, but recent progress has been made. One such CRISPR system takes advantage of a light-inducible heterodimerizing Cas9 protein (Polstein and Gersbach, 2015). Inducible systems would be ideal for overexpression of genes like FT in cassava which requires controlled expression. Overall, these studies point towards possible applications of CRISPR/Cas9 in the induction of flowering in cassava.

The molecular mechanism of exactly how the causal viruses (MCMV and SCMV) together cause the MLN disease is not yet known. Regardless, if a large-effect QTL for MLN resistance is identified and validated, then it could be fine-mapped to identify the underlying gene. Genome editing could recreate appropriate favorable polymorphisms in the MLN-susceptible maize lines. However, the challenge is to edit the exact causal allele in the susceptible but elite maize lines, especially parents of popular commercial hybrids in Africa, and create resistant versions directly. Another potential route is to use a translational approach: identify maize orthologs of the genes for virus resistance from other crop species and edit them to determine whether they confer resistance against MLN.

Conventional plant breeding involves crossing an elite, commercial line (as a recurrent parent) to a donor parent (with MLN resistance) and then backcrossing over many cycles to recover the recurrent parent genome while introgressing the trait of interest from the donor parent. Backcrossing is a resource-intensive and time-consuming process. Even after eliminating a substantial proportion of the donor genome in the converted elite line, some of the not-so-desirable genes from the donor parent continue to be present, leading to unpredictable effects on agronomic performance. For example, after four backcrosses, ∼3% of the donor genes continue to persist in the converted line (Dhugga, 2022). Genome editing directly in elite, commercial but susceptible lines could eliminate the need for continued backcrossing, saving resources, speeding up product delivery, yet at the same time sparing the converted line the yield drag that accompanies backcrossing.

As most of the hybrids grown in Africa are three-way crosses, all three lines for each hybrid would require the introduction of the recessive resistance allele. CIMMYT focused on a large-effect QTL for resistance against MLN from an exotic maize line, KS23-6, which was validated in several populations derived from its crosses with CIMMYT lines (Murithi et al., 2021). The QTL mapped near the telomere of the long arm of chromosome 6 (Figure 4). In partnership with Corteva Agriscience and under a grant from Bill and Melinda Gates Foundation (BMGF), CIMMYT has fine mapped this QTL to a ∼100 kb genetic interval (Boddupalli et al., 2020). Recessive inheritance suggests either a loss of function, which could result from an inactive form of the corresponding protein required by the virus for its replication or movement, or an altered protein sequence with a different conformation, which the virus is unable to recognize.

Maize lines susceptible to MLN were edited using CRISPR/Cas9 technology targeting the candidate genes for MLN resistance. After an outcross to the unedited parent and simultaneous screening for unintended changes in the genome with highly sensitive molecular tools, the lines are ready to be tested in the field (Zastrow-Hayes et al., 2015). The major QTL for MLN resistance identified in KS23-6 could act as a background source of resistance or could be directly created in other genetic backgrounds to further fortify their partial MLN resistance.

Deletion of various parts of the 100 kb genetic interval where the KS23-6 QTL for MLN resistance resides should allow identification of the causal polymorphism. Once validated, the causal gene could be directly edited in the CIMMYT lines, followed by reconstitution of the original three-way hybrids.

A translational approach by transferring knowledge on virus resistance from other plant species to maize is another avenue to improve resistance against MLN. Viruses are known to hijack their host’s protein translation machinery to replicate themselves. The host could become resistant if one or more of the components that virus hijacks is mutated (Sanfacon, 2015; Miras et al., 2017). Eukaryotic translation initiation factors (eIF) and two types of elongation factors have been reported to be recruited by the viruses to translate their RNA in plant species (Riis et al., 1990; Jackson et al., 2010). Mutants in several of them are known to confer resistance (Sanfacon, 2015). No eIF has yet been reported for virus resistance in maize, which has more than 25 eIF genes. An option is to use phylogenetic analysis to identify the maize orthologs of the genes from other plant species where they are known to be involved in virus resistance and then knock them out using SDN1 to determine whether and which ones confer resistance to MLN.

Tropical maize lines require 5–6 months in the greenhouse for each generation. In contrast, a fast-flowering line, referred to as mini-maize, cycles from seed to seed in 2 months (McCaw et al., 2016). Mini-maize is highly susceptible to MLN, providing a tool to expeditiously test genes for MLN resistance. Once the efficacious genes are identified, they could be altered directly in commercial CIMMYT lines.

Striga is a genus of parasitic plants that significantly limits agricultural production in Africa. Particularly, two species, S. hermonthica, and S. asiatica, limit sorghum and other cereal production in SSA. Currently, about two-thirds of the farmland under cultivation is infested with one or more species of Striga, directly impacting over 300 million peasant farmers in over 25 countries with yield losses of USD 7 billion annually (Ejeta, 2007).

The parasite is hard to manage because of its well-adopted parasitic lifestyle (Runo and Kuria, 2018). Current control strategies used for Striga management are based on cultural practices (e.g., crop rotation, intercropping/trap crops, different planting techniques, hand weeding, management of soil fertility), use of herbicide containing seed dressing, and direct chemical treatment of soil to reduce seed levels in the soil, and identification of resistant or tolerant varieties (Kanampiu et al., 2018). These methods are either ineffective or too expensive for smallholder farmers in Africa. Experts agree that effective control of parasitic plants can only be achieved through an integrated approach that highly exploits host-based resistance (Mwangangi et al., 2021). Modern techniques make such an approach feasible because of the increasing knowledge of the genetic mechanisms that underpin Striga-host interactions. Such advances can be combined with versatile genome editing tools to introduce host-based resistance against the parasite.

In our view, current opportunities for controlling Striga using genome editing point to three possibilities that hinge on interfering with the communication exchange that is intricately coupled between Striga and its hosts. The first approach could be developing Striga resistance by uncoupling Striga-sorghum interactions during germination and haustorium formation. Striga’s life cycle begins with germination induced by chemical cues produced by the host root exudate called strigolactones (Matusova et al., 2005; Gomez-Roldan et al., 2008). Subsequently, the parasite develops a specialized organ (haustorium) using chemical cues from the host referred to as haustorium inducing factors (HIFs) (Bandaranayake et al., 2010; Wada et al., 2019). Host triggered germination and haustorium induction represent the pre-attachment stages of the parasite, and hosts that “disallow” these processes to occur are said to harbor pre-attachment Striga resistance. The genetic cause of pre-attachment resistance in sorghum is due to mutations on the LOW GERMINATION LOCI 1 (LGS1). Loss of function lgs1 mutants are not effective in stimulating seeds of the parasite to germinate. Following on this information, gene-edited sorghum varieties were developed using CRISPR/Cas9 targeting the LGS1. The lgs1 mutants showed high levels of resistance against the parasite (Bellis et al., 2020).

Aside from the LGS1 loci in sorghum, other genes in the strigolactone biosynthetic pathway can be used to disrupt the flow of information from the host to the parasite. For example, (Bari et al., 2019) developed a tomato variety resistant to obligate root parasite P. aegyptica, by modifying the carotenoid cleavage dioxygenase 8 (CCD8), critical in the strigolactone biosynthesis pathway. Obliteration of CCD8 by CRISPR/Cas9 genome editing approach resulted in reduced production of orobanchol in tomato and subsequently less germination and resistance against the parasite. Similarly, (Butt et al., 2018) developed a rice variety using CRISPR/Cas9 with reduced S. hermonthica germination by targeting OsCCD7.

A second approach for Striga resistance could be uncoupling Striga-sorghum interactions mediated by host-derived susceptibility factors such as DMR6, a well-studied susceptibility gene in Arabidopsis (Damme et al., 2008). CRISPR/Cas9-mediated editing of the DMR6 gene in tomato, banana, and sweet basil showed broad-spectrum resistance against fungal and bacterial pathogens (de Toledo Thomazella et al., 2021; Hasley et al., 2021; Tripathi et al., 2021b). Mutants of DMR6 display reduced susceptibility to the pathogen. Based on these observations, one can hypothesize that Striga resistance can be achieved through uncoupling critical Striga-host interactions mediated by compatibility factors. Such a hypothesis is supported by recent findings that showed significant associations of sorghum resistance against Striga in a single nucleotide polymorphism on sorghum’s ortholog of AtDRM6 (Kavuluko et al., 2021).

Finally, it is desirable to stack multiple levels of Striga resistance for durable and broad-spectrum resistance (Figure 5). Preferably, such a strategy should target both stages of the Striga lifecycle: pre- and post-attachment resistance. To achieve stacked resistance, a two-pronged approach can be used: Firstly, by simultaneously targeting loci such as the lgs1 and dmr6 during genome editing, and secondly, by selecting and crossing products of two loci such as lgs1 and dmr6 editing. In any case, an initial detailed characterization of the mechanisms of resistance is critical.

Although sorghum is a staple food for millions of people in Africa, its grain has poor nutritional quality mainly because of low levels of essential amino acids, such as Lys, poor protein digestibility (Taylor and Schüssler, 1986; Aboubacar et al., 2001). Protein quality and digestibility is attributed to prolamins called kafirins, particularly the α – kafirin. Studies of the α-kafirin floury sorghum mutant P721Q, reveal that the genotype has low levels of α-kafirin and increased Lys (Oria et al., 2000; Wu et al., 2013). In addition, the reduced kafirin alters the protein structure to make it more accessible to gastric proteases, thereby increasing protein digestibility (Oria et al., 2000; Duodu et al., 2003; Wong et al., 2009). These studies have, therefore, made Kafirin a target for improving protein quality in sorghum. For example, RNA interference (RNAi) was used to reduce α-kafirins in sorghum (Kumar et al., 2012). More recently, a genome editing approach using CRISPR/Cas9 was used to create variants with reduced kafirin levels and improved protein quality and digestibility (Li et al., 2018).

The first demonstration of genome editing in wheat was achieved using TALENs to knockout three TaMLO homoeologs to create powdery mildew-resistant wheat (Wang et al., 2014). MLO is a susceptibility gene, and its loss of function confers durable and broad-spectrum resistance to powdery mildew in various plant species (Büschges et al., 1997). However, the knockout of the MLO gene can lead to growth penalties and yield losses. Recently, Li et al. (2022) demonstrated that Tamlo-R32, a mutant with a targeted deletion in the MLO-B1 locus, showed robust resistance to the powdery mildew disease in wheat without impacting its growth and yields.

In 2017, Zhang et al. (2017) reported using CRISPR to generate Taedr1 wheat plants by simultaneously disrupting the three homoeologs of EDR1. The resulting mutant plants were resistant to powdery mildew and did not exhibit mildew-induced cell death (Zhang et al., 2017). Cytidine-deaminase-mediated base editing has been used in wheat to create herbicide-resistant plants by generating point mutations within the acetyl-coenzyme A carboxylase (ACC) gene (Li et al., 2018).

CRISPR/Cas9 technology has been applied to wheat for improving grain quality. Low-gluten wheat was developed by targeting the a-gliadin genes (Sanchez-Leon et al., 2018). The wheat gliadin genes encode gluten proteins responsible for the celiac disease in genetically predisposed individuals. Later, wheat was edited for high-amylose targeting the TaSBEIIa gene (Li et al., 2020). The edited wheat line showed a significantly increased resistant starch content.

The yields of wheat have been improved by manipulating the negative regulatory genes. The genome-edited wheat developed by knocking out the three TaGASR7 homoeologs (TaGW2-A1, -B1, and -D1), a gibberellin-regulated gene, showed a significant increase in kernel weight compared to the control wild-type (Zhang et al., 2016). Similarly, wheat mutants with a knockout of the GW2 gene encoding a RING-type E3 ligase that controls rice grain weight demonstrated increased grain yields (Zhang et al., 2018).

Genome editing efforts towards developing disease-resistant crops have focused on gene disruption, replacement, or regulation. For instance, disrupting negative regulators of plant disease resistance such as host susceptibility (S) genes could offer durable resistance to diseases. This strategy could durably offer resistance to yam viruses by knocking out eukaryotic translation initiation factors (eIFs). In plants, eIFs are translation initiation factors that mediate the replication of plant RNA viruses, majorly potyviruses (Michel et al., 2019). Therefore, targeting these gene in yam could curb potyvirus infestations such as yam mosaic virus, as reported in cassava (Gomez et al., 2019) and cucumber (Chandrasekaran et al., 2016; Macovei et al., 2018). On the other hand, yam badnaviruses could be managed by targeting viral sequences integrated in host plant genomes, as demonstrated in banana (Tripathi et al., 2019b).

Susceptibility genes, mainly the mildew locus O (MLO), enhanced disease resistance 1 (EDR1), and the Non-Expressor of Pathogenesis-Related 3 (NPR3), could also represent good genome editing targets for generating resistance to fungal diseases in yam (Syombua et al., 2021). Since the fungal disease anthracnose is the most widespread foliar disease in yam (Amusa et al., 2003), developing endogenous resistance would alleviate the associated yield losses, ensuring food security for an economically disadvantaged population. Moreover genes that are highly conserved across plant species and have successfully generated plant fungal resistance, such as WRKY transcription factors and ERF922, could be precisely modified to achieve these endeavors (Noman et al., 2020). The precise modification of host susceptibility genes such as DMR6 and SWEET could be affected to confer food yam with resistance to bacterial diseases. Further, the upregulation of host resistance genes is also a feasible approach for generating disease-resistant yam lines (Sameeullah et al., 2017).

Various abiotic stress factors, including declining soil fertility and unpredictable weather patterns such as floods, drought, and high temperatures, are critical constraints to sustainable yam production, resulting in substantial yield losses. Considering that yam growing regions span a wide range of agro-ecological zones that include marginalized lands (Frossard et al., 2017), there is a need to develop yam accessions with better adaptability to these conditions that can flourish in soils with reduced nutrient profiles. Gene function analyses in various crops have unveiled numerous differentially expressed genes following plant exposure to different abiotic stress conditions. In cassava, for instance, Ou et al. (2018) demonstrated that exposing cassava plants to high salinity levels, low-temperature pressure, and reduced water content upregulates the expression of KUP genes. Therefore, KUP and other gene orthologues in yam that are crucial for plant response to various stress conditions could be precisely modified to generate yam lines tolerant to stress conditions. Some of these genes include heat shock factors (HSFs), mitogen-activated protein kinases (MAPKs), ethylene response factors (ERFs), MYB, and WRKYs (Jaganathan et al., 2018; Syombua et al., 2021).

Yam production is generally a labor-intensive venture due to staking and weed competition requirements. Weeds directly compete with crops for access to light, water, and soil nutrients, thus reducing the yields. Besides, weeds could act as pathogen reservoirs, increasing the disease risk to yam plants. It is, therefore, important to develop environment friendly and economically sustainable strategies for weed management in yam plantations (Dentika et al., 2021). The development of gene-edited herbicide-tolerant yam accessions can effectively alleviate the weed challenge while alleviating crop phytotoxicity due to the reduced need for repeated use of chemical herbicides. Among the potential target gene orthologues in yam include the EPSPS (5-enolpyruvylshikimate-3-phosphate), ACCase (acetyl-coenzyme A carboxylase), ALS (acetolactate synthase) genes (Dong et al., 2021). As Syombua et al. (2021) discussed, genome engineering strategies also hold immense potential for improving the yield and nutritional quality of yams.