Principal investigators:

Prof. Dr. Thomas Lahaye,

Universität Tübingen,

ZMBP, Allgemeine Genetik,

Auf der Morgenstelle 32, 72076 Tübingen,

Tel 07071 - 2972076

Fax 07071 - 295042

thomas.lahayespam prevention@zmbp.uni-tuebingen.de

Prof. Dr. Thilo Stehle,

Universität Tübingen,

IFIB, Strukturbiologie,

Hoppe-Seyler-Str. 4, 72076 Tübingen,

Tel 07071 – 29 73043

Fax 07071 – 29 5565

thilo.stehlespam prevention@uni-tuebingen.de

Summary:

The pepper resistance (R) gene Bs3 is transcriptionally activated by the Xanthomonas transcription activator-like effector (TALE) AvrBs3. Bs3 is a structurally unique plant R protein that triggers cell death by unknown means. Bs3 is most related to YUCCAs, a plant-specific family of flavin-dependent monooxygenases (FMOs) that induce cell proliferation but not cell death. YUCCAs bind NADPH₂ and O₂ to convert indole-3-pyruvate (IPA) into Indole-3-acetic acid (IAA). Alternatively, YUCCAs transfer reduction equivalents to O₂ resulting in H₂O₂. In planta expression of Bs3 causes increased H₂O₂- but not IAA-levels, suggesting that Bs3 triggers cell death via H₂O₂ production. In support of this model, recombinant Bs3 produces 5‑fold more H₂O₂ than Arabidopsis YUCCA6, a YUCCA representative. Yeast two-hybrid (Y2H) identified the Arabidopsis transcription factor TEOSINTE BRANCHED1/CYCLOIDEA/PCF9 (TCP9) as Bs3 interactor. DNA binding of TCP proteins is redox-regulated and TCP9 activates isochorismate synthase, a key enzyme of salicylic acid (SA) synthesis. Bs3-triggered cell death correlates with an increase in SA, in agreement with a model in which H₂O₂ produced by Bs3 activates TCP9. We aim to elucidate functional differences of Bs3 and YUCCA and pinpoint causal polymorphic residues. Furthermore, we aim to identify and study components that Bs3 utilizes to trigger cell death. These studies will provide the first insights into the molecular function of Bs3. Furthermore these studies will clarify whether Bs3 employs novel or known components of plant immune pathways.