Poster
Ayaka Yoshihisa
Kindai University
Nara City, Nara, Japan
Satomi Yoshimura
Kindai University
Nara, Nara, Japan
Kei Nishikawa
Kindai University
Nara, Nara, Japan
Motoki Shimizu
Iwate Birotechnology Research Center
Kitakami, Iwate, Japan
Masatsugu Toyota
Saitama University
Saitama, Saitama, Japan
Koji Yamaguchi
Kindai University
Nara, Nara, Japan
Tsutomu Kawasaki
Kindai University
Nara, Nara, Japan
Bacterial blight disease, the most important disease in rice, is caused by Xanthomonas oryzae pv. oryzae (Xoo). The rice cultivar Kogyoku possesses the nuclear-localized CC-BED-NB-LRR type receptor Xa1, which recognizes the transcription activator-like effector (TALE) secreted by Xoo into plant cell, and then induces a hypersensitive response accompanied by cell death. However, the molecular mechanism underlying Xa1-mediated immunity remains unclear. Previously, we identified the rice transcription factor OsERF101, which interacts with both Xa1 and TALE. OsERF101 functions as a positive regulator in Xa1-dependent immunity. The BED domain of Xa1 was found to interact with OsERF101. In addition, Xa1-induced cell death was suppressed by disrupting the interaction between the BED domain and OsERF101. These results suggest that Xa1 recognizes TALE through the interaction between OsERF101 and TALE. Furthermore, we discovered that upon TALE recognition by Xa1, Ca2+ influx occurred in the nucleus. Xa1-induced cell death was significantly inhibited by treatment of Ca2+ channel inhibitor LaCl3. Therefore, it is likely that Xa1 induces Xoo resistance through nuclear Ca2+ influx. Blue-native PAGE experiments revealed that Xa1 forms a high-molecular-weight complex in the steady state. We are currently investigating the dynamic changes in the Xa1 protein complex upon TALE recognition.