Ectopic activation of the rice NLR heteropair RGA4/RGA5 confers resistance to bacterial blight and bacterial leaf streak diseases

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Hutin, Mathilde | Cesari, Stella | Chalvon, Véronique | Michel, Corinne | Tran, Tuan Tu | Boch, Jens | Koebnik, Ralph | Szurek, Boris | Kroj, Thomas, T.

Edité par CCSD ; Wiley -

BGPI : Equipe 4 : Interactions Céréales Agents Pathogènes (ICAP). International audience. Bacterial Blight (BB) and Bacterial Leaf Streak (BLS) are important rice diseases caused,respectively, by Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola(Xoc). In both bacteria, Transcription Activator-Like (TAL) effectors are major virulencedeterminants that act by transactivating host genes downstream of Effector-Binding Elements(EBEs) bound in a sequence specific manner. Resistance to Xoo is mostly related to TALeffectors action, either by polymorphisms that prevent induction of susceptibility (S) genes orby executor (R) genes with EBEs embedded in their promoter and that induce cell death andresistance. For Xoc, no resistance sources are known in rice. Here, we investigated whether therecognition of effectors by nucleotide-binding and leucine rich repeat domain immunereceptors (NLRs), the most widespread resistance mechanism in plants, is also able to stop BBand BLS. In one instance, transgenic rice lines harboring the AVR1-CO39 effector gene from therice blast fungus Magnaporthe oryzae, under the control of an inducible promoter, werechallenged with transgenic Xoo and Xoc strains carrying a TAL effector designed to transactivatethe inducible promoter. This induced AVR1-CO39 expression and triggered BB and BLSresistance when the corresponding Pi-CO39 resistance locus was present. In a second example,transactivation of an auto-active NLR by Xoo-delivered designer TAL effectors resulted in BBresistance, demonstrating that NLR-triggered immune responses efficiently control Xoo. Thisforms the foundation for future BB and BLS disease control strategies whereupon endogenousTAL effectors will target synthetic promoter regions of Avr or NLR executor genes.

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