Poster
Niels Gallas
PhD Student
ZMBP, University of Tuebingen
Reutlingen, Baden-Wurttemberg, Germany
Tom Schreiber
Leibniz Institute of Plant Biochemistry
Halle (Saale), Sachsen-Anhalt, Germany
Robert Morbitzer
ZMBP, University of Tuebingen
Tuebingen, Baden-Wurttemberg, Germany
Kenneth W. Berendzen
ZMBP, University of Tuebingen
Tuebingen, Baden-Wurttemberg, Germany
Paulo Teixeira (he/him/his)
Assistant Professor
University of Sao Paulo/
Piracicaba, Sao Paulo, Brazil
Alain Tissier
Head of Institute
Leibniz Institute of Plant Biochemistry
Halle, Sachsen-Anhalt, Germany
Thomas Lahaye
Eberhard-Karls-University Tübingen
Tuebingen, GERMANY
Xanthomonas manipulates host plants by injecting TALEs that bind target gene promoters and activate transcription. TALEs interact with the general transcription factor TFIIAγ to recruit the RNA pol II complex, enabling them to create a shortcut in eukaryotic transcription without the need of other transcription factors and the mediator complex. In an EMS-screen, we identified a pepper plant (C. annuum) that is insensitive to TALEs. Mapping suggested a SNP that changed a single residue (D42N) in TFIIAγ as the causal mutation. Interestingly, not only TALEs but also RipTALs from Ralstonia were affected, despite sharing little homology to TALEs. For further analysis, we used a novel, precise editing approach that enables scarless knock-ins in Arabidopsis and tomato. We used this technology to introduce TFIIAγ polymorphisms into the tomato genome. Genotyping confirmed scar-free knock-ins in endogenes and edited plants that carried the TFIIAγ polymorphisms D42N or V39E (originating from rice xa5) showed a drastically reduced response to TALEs and RipTALs, strongly suggesting that these plants might be resistant to bacteria that use TALEs for susceptibility. Overall, we showed that precise editing by knock-in is feasible in tomato and this novel technology can be used to edit plant genomes at unprecedented levels. Our work highlights the importance of TFIIAγ for TALE-based manipulation of the host while TFIIAγD42N expands the possibilities of a TFIIAγ-based resistance beyond xa5.