With respect to the importance of TALEs in the Rice-
We identified and characterized TalD and TalI as two African
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Abstract Background Xanthomonas oryzae pv.oryzae (Xoo ) causes bacterial leaf blight, a devastating disease of rice. Among the type-3 effectors secreted byXoo to 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 .Results Xoo pathosystem, 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 ninetal genes of the avirulent African strain MAI1 into the virulent Asian strain PXO99A, four were found to trigger resistance on specific rice accessions. Loss-of-function mutational analysis further demonstrated theavr activity of two of them,talD andtalI, 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 AfricanXoo specifically, including CT13432, could be suppressed or largely suppressed by trans-expression of the truncTALEtal2h , similarly to resistance conferred by theXa1 gene which recognizes TALEs generally independently of their activation domain.Conclusion Xoo TALEs with avirulence activity on IR64 and CT13432 respectively. Resistance of CT13432 against AfricanXoo results 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. -
null (Ed.)Vascular plant pathogens travel long distances through host veins, leading to life-threatening, systemic infections. In contrast, nonvascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and nonvascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and nonvascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the family Xanthomonadaceae and absent in most nonvascular species. CbsA expression allowed nonvascular Xanthomonas to cause vascular blight, while cbsA mutagenesis resulted in reduction of vascular or enhanced nonvascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple nonvascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits.more » « less
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Summary Plant breeders have developed crop plants that are resistant to pests, but the continual evolution of pathogens creates the need to iteratively develop new control strategies. Molecular tools have allowed us to gain deep insights into disease responses, allowing for more efficient, rational engineering of crops that are more robust or resistant to a greater number of pathogen variants. Here we describe the roles of
SWEET andSTP transporters, membrane proteins that mediate transport of sugars across the plasma membrane. We discuss how these transporters may enhance or restrict disease through controlling the level of nutrients provided to pathogens and whether the transporters play a role in sugar signaling for disease resistance. This review indicates open questions that require further research and proposes the use of genome editing technologies for engineering disease resistance.
