**8. Major techniques for inducing biotic stress resistance**

The route maps followed for a trait improvement particularly stress resistance, both biotic and abiotic remain the same. The **Figure 1** graphically depicts various tools and techniques that can be utilized with efficient and effective manner for tackling different biotic stresses in wheat.

#### **Figure 1.**

*Some major tools and techniques (both in use and under exploration) in wheat breeding for biotic stress resistance.*

### **9. Present scenario**

#### **9.1 Fungal diseases**

So far, more than 240 rust resistance genes have been characterized and formally designated in wheat or its relatives; most being race-specific resistance genes. At least 67 of these genes are designated as *Sr* resistance genes [105, 114, 115]. *Sr31* was one of the most widely utilized race-specific *Sr* resistance genes [116]; however, its presence at the International Maize and Wheat Improvement Center (CIMMYT) has been drastically reduced following testing against Ug99 races in Kenya. Evolution of virulence against *Sr31* with the emergence of Ug99 led to stem rust susceptibility in most of the wheats grown around the globe. After its new races overcame a number of resistance genes, the genes *Sr2*, *Sr23*, *Sr25*, *Sr33*, *Sr35*, *Sr45*, *Sr47*, and *Sr50* are presently the most efficient for protection against newly evolved races [117]. The QTL-controlling stripe rust resistance in *T. monococcum* was mapped on chromosome 2A (*QYrtm.pau-2A*), whereas the QTL from *T. boeoticum* was mapped on 5A (*QYrtm. pau-5A*). One stripe rust-resistant gene from *T. boeoticum* acc. pau5088 was confirmed to be introgressed in cultivated wheat which was indicated by co-introgression of *T. boeoticum* sequences linked to stripe rust-resistant QTL, *QYrtb.pau-5A* [118].

For stripe (yellow) rust resistance, 95 genes have been characterized and formally named [105, 114, 115]. However, most of these genes have been rendered ineffective with emergence of virulent races around the globe with exception of a few combinations, such as the combination of *Yr5* and *Yr15* that remain effective worldwide. At Punjab Agricultural University, Ludhiana, India, about 200 accessions of *T. monococcum* and *T. boeoticum* were screened for leaf rust and stripe rust

#### *Breeding Wheat for Biotic Stress Resistance: Achievements, Challenges and Prospects DOI: http://dx.doi.org/10.5772/intechopen.97359*

resistance for several years and we found that all the *T. monococcum* accessions, most of the *T. boeoticum* and a few *T. urartu* accessions, were completely resistant to leaf rust. However, a lot of variation was observed for stripe rust resistance. Leaf and stripe rust resistance genes have also been introgressed from diploid species *Ae. umbellulata* and *Ae. caudata* using *T. durum* as bridging species [118, 119].

Similarly, 80 *Lr* resistance genes have been genetically characterized and documented [115]. Out of these, *Lr1*, *Lr3*, *Lr10*, and *Lr20* have been commonly deployed in wheat cultivars [120]. Generally, ASR genes are rendered ineffective with continual emergence of new virulent races of rust pathogens through mutation and recombination [121]. It has been well documented through cloning of 11 racespecific genes in wheat (*Sr22*, *Sr33*, *Sr35*, *Sr45*, *Sr50*, *Yr5*, *Yr10*, *Lr1*, *Lr10*, *Lr21*, and *Lr22*) that these genes encode NLR proteins [122–126].

Till date, only seven race non-specific APR genes have been genetically characterized and formally designated in wheat namely *Sr2*/*Yr30*, *Lr34*/*Yr18*/*Sr57*/*Pm38*, *Lr46*/*Yr29*/*Sr58*/*Pm39*, *Lr67*/*Yr46*/*Sr55*/*Pm46*, *Lr68*, *Sr56*, and *Yr36* [127–133]. Cloning of the APR genes *Yr36*, *Lr34*/*Yr18*/*Sr57*/*Pm38* and *Lr67*/*Yr46*/*Sr55*/*Pm46* has revealed the roles of cytoplasmic protein kinase, adenosine triphosphate (ATP)-binding cassette transporter, and hexose transporter, respectively in mediating resistance [134–136].

Growing resistant cultivars is the most cost-effective strategy for tackling PM. To date, 70 PM resistance genes have been formally cataloged; most of these provide race-specific resistance in wheat [114, 115]. It is desirable to know the virulence pattern of isolates to generate effective combinations of race-specific resistance genes [137]. More effective method would be deployment of combinations of race non-specific resistance genes is a promising method. As discussed above in the section for rust resistance, only three race non-specific resistance genes have been identified, out of which two pleiotropic genes (*Lr34*/*Yr18*/*Sr57*/*Pm38* and *Lr67*/*Yr46*/*Sr55*/*Pm46*) have been cloned [135, 136].

Genetic resistance to FHB is mainly quantitative and is controlled by multiple moderate to minor genes [138]. Although genetic resistance is the most costeffective method, it is hard to accomplish in commercial cultivars due to its complex behavior. This complexity is further enhanced by various resistance mechanisms, e.g., invasion (type I), fungal spread (type II), toxin accumulation (type III), kernel infection (type IV) and yield reduction (type V) [139]. FHB resistance also displays significant correlations with heading, plant height, and anther extrusion of the wheat plant [140]. To date, seven genetic loci designated as *Fhb1*, *Fhb2*, *Fhb4* and *Fhb5* from wheat, and *Fhb3*, *Fhb6* and *Fhb7* from wild relatives, have been formally named as FHB resistance genes [141]. The cultivars Sumai 3 from China and Frontana from Brazil have been identified as sources of moderate resistance to FHB**.**

Karnal bunt is among the few quarantine diseases that restrict free trade among countries due to quarantine regulations [142]). Resistance to Karnal bunt has been reported in durum wheat (*Triticum turgidum*), common wheat, *Aegilops*, rye and barley under artificial conditions [143, 144]. Susceptibility of *T. aestivum* to Karnal bunt might be due to presence of an additional D genome [145, 146]. Sharma et al. [147] at PAU developed high yielding Karnal bunt resistant wheat lines by introgression of Karnal bunt resistance from KBRL 22 into the background of high yielding PBW343. Studies on deciphering genetics of resistance have indicated the presence of quantitative rather than qualitative resistance [145, 146, 148]. Fuentes-Davila et al. [145] suggested six genes, designated Kb1, Kb2, Kb3, Kb4, Kb5, and Kb6, while Villareal et al. [149] postulated a minimum of three genes for resistance. Studies on deciphering genetics of resistance have indicated the presence of quantitative rather than qualitative resistance [145, 148].

For loose smut**,** the majority of genetic studies carried out thus far have demonstrated simple inheritance with one, two or three major genes in hexaploid wheat

controlling resistance to several races of *U. tritici*. The first four loose smut resistance genes *Ut1* to *Ut4* were named based on segregation of avirulence in *U. tritici* [150, 151]. Genes *Ut1* and *Ut3* have no chromosome assignment. Based on pedigree, the gene symbol *Ut2* was assigned to the resistance gene on chromosome 6A to race T19 [152]. *Ut4* associated with the Thatcher derived differential line TD12A, was located on chromosome 7B [153, 154]. *Ut5* was located on chromosome 2BL [155], *Ut6* was initially reported on chromosome 5B by Kassa et al. [156] which was later validated by Knox et al. [153]. A gene located to chromosome 7A by Dhitaphichit et al. [157] was subsequently named *Ut7* [153]. Knox et al. further identified genes *Ut8* on chromosome 3A, *Ut9* on chromosome 6B and *Ut10* on chromosome 6D. Several studies revealed the additive nature of resistance genes, while in some cases, duplicate complementary action of multiple genes was also implicated [158].

Finally, the genetic resistance to wheat blast at the seedling stage follows a genefor-gene interaction model [159] and five resistance genes namely *Rmg2, Rmg3, Rmg7, Rmg8*, and *RmgGR119* have been identified in wheat against the *Magnaporthe oryzae* pathotype *triticum* [160–164].

Various molecular markers have been widely used to tag and map resistance genes in wheat; however, SSRs have emerged as the choice of marker in gene-mapping studies. These markers can be strategically used for selection of desirable gene combinations along with phenotypic assays. Wheat has more than 3000 SSR markers mapped so far [165]. Molecular markers can be used for alien gene transfers and understanding the mechanism of gene transfer. Such markers ensure selection of a target gene based on the presence of the linked genotype. The success of selection depends on the close genetic association and robustness of a given marker across different genetic backgrounds. At PAU, a number of genes/QTLs have been mapped for different wheat diseases including stripe rust, cereal cyst nematode, and Karnal bunt. Two QTLs, one each in *T. monococcum* acc. pau14087, and *T. boeoticum* acc. pau5088, were detected for resistance in the RIL population. The QTL in *T. monococcum* mapped on 2A in a 3.6 cM interval between *Xwmc407* and *Xwmc170*, whereas the QTL from *T. boeoticum* mapped on 5A in 8.3 cM interval between *Xbarc151* and *Xcfd12* [166–168].

### **9.2 Insect-pests**

In the last 50 years or so, the HPR concept has been extended to insect-host interactions. As a result, insect resistant cultivars are now in the picture. The variables, both biotic and abiotic which play a major role in deciding the plant reaction to pest, along


#### **Table 3.**

*Genes identified for insect resistance in wheat and their respective categories.*

#### *Breeding Wheat for Biotic Stress Resistance: Achievements, Challenges and Prospects DOI: http://dx.doi.org/10.5772/intechopen.97359*

with mechanisms and categories of resistance are now better understood. Drawing analogy from plant-pathogen interactions, pest-host relationships are now being viewed as (susceptible plant) and incompatible (resistant plant) interactions [74].

Deployment of insect resistance genes in wheat along with other field crops has increased steadily over the years from mid 60s. Marker assisted selection (MAS) and breeding has sped up the process of identification of resistance loci and QTLs and understanding of the mechanisms governing the resistance. **Table 3** depicts the genes identified for insect resistance in wheat and their respective categories.
