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Xanthomonas oryzaepv.oryzae(Xoo) causes bacterial leaf blight, a devastating disease of rice. Among the type-3 effectors secreted byXooto support pathogen virulence, the Transcription Activator-Like Effector (TALE) family plays a critical role. Some TALEs are major virulence factors that activate susceptibility (S) genes, overexpression of which contributes to disease development. Host incompatibility can result from TALE-induced expression of so-called executor (E) genes leading to a strong and rapid resistance response that blocks disease development. In that context, the TALE functions as an avirulence (Avr) factor. To date no such avirulence factors have been identified in African strains ofXoo.

With respect to the importance of TALEs in the Rice-Xoopathosystem, we aimed at identifying those that may act as Avr factor within AfricanXoo. We screened 86 rice accessions, and identified 12 that were resistant to two African strains while being susceptible to a well-studied Asian strain. In a gain of function approach based on the introduction of each of the ninetalgenes of the avirulent African strain MAI1 into the virulent Asian strain PXO99^A, four were found to trigger resistance on specific rice accessions. Loss-of-function mutational analysis further demonstrated theavractivity of two of them,talDandtalI,on the rice varieties IR64 and CT13432 respectively. Further analysis of TalI demonstrated the requirement of its activation domain for triggering resistance in CT13432. Resistance in 9 of the 12 rice accessions that were resistant against AfricanXoospecifically, including CT13432, could be suppressed or largely suppressed by trans-expression of the truncTALEtal2h, similarly to resistance conferred by theXa1gene which recognizes TALEs generally independently of their activation domain.

We identified and characterized TalD and TalI as two AfricanXooTALEs with avirulence activity on IR64 and CT13432 respectively. Resistance of CT13432 against AfricanXooresults from the combination of two mechanisms, one relying on the TalI-mediated induction of an unknown executor gene and the other on anXa1-like gene or allele.