The spot blotch disease of wheat is caused by Bipolaris sorokiniana , which is an anamorph (teleomorph Cochliobolus sativus ). The disease mainly occurs in warm, humid wheat‐growing regions, and the Eastern Gangetic Plains ( EGP ) of South Asia is a hotspot. Significant progress has been made in recent years in characterizing the host–pathogen interaction. The study of the pathogen's life cycle and diversity have been an active area of research. A number of resistance sources have also been identified, characterized and used for breeding. Although immunity has not been observed in any genotype, cultivars displaying a relatively high level of resistance have been developed and made available to farmers. Further progress will require regular use of marker‐assisted breeding, genomic selection, gene editing and transgenic interventions. This review summarizes the current state of knowledge about genetic and breeding efforts on the wheat– B. sorokiniana pathosystem and discusses ways in which emerging tools can be used for future research to understand the mechanism involved in infection and for developing cultivars exhibiting a high level of resistance.

The ToxA–Tsn1 system is an example of an inverse gene-for-gene relationship. The gene ToxA encodes a host-selective toxin (HST) which functions as a necrotrophic effector and is often responsible for the virulence of the pathogen. The genomes of several fungal pathogens (e.g., Pyrenophora tritici-repentis, Parastagonospora nodorum, and Bipolaris sorokiniana) have been shown to carry the ToxA gene. Tsn1 is a sensitivity gene in the host, whose presence generally helps a ToxA-positive pathogen to cause spot blotch in wheat. Cultivars lacking Tsn1 are generally resistant to spot blotch; this resistance is attributed to a number of other known genes which impart resistance in the absence of Tsn1. In the present study, 110 isolates of B. sorokiniana strains, collected from the ME₅A and ME₄C megaenvironments of India, were screened for the presence of the ToxA gene; 77 (70%) were found to be ToxA positive. Similarly, 220 Indian wheat cultivars were screened for the presence of the Tsn1 gene; 81 (36.8%) were found to be Tsn1 positive. When 20 wheat cultivars (11 with Tsn1 and 9 with tsn1) were inoculated with ToxA-positive isolates, seedlings of only those carrying the Tsn1 allele (not tsn1) developed necrotic spots surrounded by a chlorotic halo. No such distinction between Tsn1 and tsn1 carriers was observed when adult plants were inoculated. This study suggests that the absence of Tsn1 facilitated resistance against spot blotch of wheat. Therefore, the selection of wheat genotypes for the absence of the Tsn1 allele can improve resistance to spot blotch.

Marker assisted backcrossing (MABC) was used to transfer the three stem rust (Puccinia graminis tritici) resistant genes Sr25, SrWeb and Sr50 into the popular Indian wheat cv. HUW234. The donor was the CIMMYT breeding line PMBWIR4, and each of the target genes was marked by a simple PCR assay. A three step screening strategy was adopted: the first screen comprised foreground selection, the second used markers lying close to the introgression borders to reduce the extent of linkage drag, and the last was background selection based on 149 informative microsatellite assays. Based on the background selection outcomes, at the BC1F1 generation the proportion of the genome fixed for cv. HUW234 alleles ranged from 55% to 67%. Three BC1F1 individuals were crossed a second time with cv. HUW234, resulting in the identification of six BC2F3 families carrying all three target Sr genes; the proportion of their genome inherited from cv. HUW234 ranged from 86% to 92%. BC2F4 and BC2F5 material was planted at three different locations under both disease-free and artificially induced epiphytotic conditions. Compared to recurrent parent, the improved versions of cv. HUW234 displayed significantly superior resistance to stem rust, and their agronomic performance was as good as, or even marginally better than that of the source cultivar