**Acknowledgements**

*Protecting Rice Grains in the Post-Genomic Era*

**6. Resistance effectiveness**

to clone and characterize genes underlying these *R* QTLs.

Thus far, major sheath blight *R* genes have not been identified. However, the major sheath blight *R* QTL *qShB9-2* responsible for 24.3–27.2% of phenotypical variation using microchamber and mist chamber assays, respectively, and other nine minor *R* QTLs to sheath blight were also identified [58, 59]. These sheath blight *R* QTLs were verified with replicated field plot experiments in multiple locations [60]. This demonstrated that there exist useful genetic factors that can be used for breeding. DNA markers linked to these *R* QTLs can not only be used to pyramid resistance into new rice varieties via marker-assisted breeding but can also be used

*M. oryzae* is a hemi-biotrophic organism with an extended period of biotrophic invasion that forced the evolution of robust major blast *R* genes in host. The resistance mediated by major blast *R* genes follows the gene-for-gene model where the *R* genes in rice detect the corresponding *AVR* genes in *M. oryzae* in triggering resistance responses [61]. The existence of *AVR-Pita1* in US blast populations suggest that *AVR-Pita1* may play an important role in fitness and pathogenicity. Ironically, what is needed for pathogens to survive also makes the pathogen less virulent and fit. This never-ending booming-and-busting cycle of host-pathogen interactions presents a unique opportunity to develop durable resistance. In the Southern US, after the blast epidemics in 1980s, a blast-resistant rice variety Katy was released in 1990 [62]. Katy contains a cluster of major *R* genes at the *Pi-ta* locus from the landrace indica variety Tetep and *Piks* from tropic variety Newbonnet [41]. Further analysis of Katy revealed that there are three linked blast *R* genes, *Pi-ta* and *Pi-ta2/Ptr* genes near the centromere of rice chromosome 12. *Pi-ta* is a classical *R* gene with NBS-LRR [63] and *Ptr*, which is allelic to *Pi-ta2*, encodes a predicted protein with four armadillo repeats [52]. *Ptr* was shown to confer resistance to a wide range of blast races except for IE1k and help *Pi-ta* with unknown mechanisms [52]. To date, a handful of rice varieties with the *Pita*, *Pita2/Ptr* cluster in a linkage block including Katy, Drew, Madison, Kaybonnet, Cybonnet, Banks, Ahrent, Catahoula, and Templeton have been released in the Southern US since 1990 [64–66]. Amei and colleagues showed that the *Pi-ta* gene has been bred into cultivated species of rice for decades [67]. The counter resistance from the pathogen usually occurs after breeders release a new resistant rice variety [68]. One of the counter resistance strategies of *M. oryzae* is to alter the structural integrity and expression of the *AVR* genes. The blast races (isolates) with partial, complete deletions, point mutations altering amino acids, and transposon insertions at the *AVR-Pita1* locus have been found in commercial rice fields in the Southern US since the release of *Pi-ta* [16–18]. The resistance mediated by the *Pi-ta/Pi-ta2/Ptr* gene cluster has been stable for over two decades. Consistently, most blast populations were found to carry *AVR-Pita1* [16–18] that verified the durability of resistance mediated by *Pi-ta/Pi-ta2/Ptr*. The observed resistance durability could be due to the lack of deployment of rice cultivars with the *Pi-ta/Pi-ta2/Ptr* genes to force the loss of *AVR-Pita1*. This is consistent with the fact that limited *Pi-ta/Pi-ta2/Ptr* containing rice varieties have been grown due to moderate yield advantages compared to other rice varieties lacking the genes since their releases [69]. Alternatively, it is also fully possible that *AVR-Pita1* is important for the survival of *M. oryzae* with unknown mechanisms.

In the USA, any rice cultivar with one or two major blast *R* genes will continue to be effective to prevent rice blast disease. On the other hand, a combination of major

**46**

**7. Summary**

The authors thank Michael Lin, Tracy Bianco, Heather Box, Alan Sites, and Laduska Sells of USDA ARS DBNRRC and Mary Jia of Arkansas Schools of Math, Sciences and the Arts; Dr. Guangjie Liu of University of Arkansas Rice Research and Extension Center for excellent technical assistance; and Tyler Franzen for a photo taken by a drone. Special thanks are also given to all other scientists and supporting staff members of DB NRRC, and UA RREC for their continued support and useful discussion and interactions with the Molecular Plant Pathology program. For critical reviews we thank Drs. Trevis Huggins and Yong-Bao Pan of USDA ARS and two anonymous reviewers. USDA is an equal opportunity provider and employer.
