OsRap2.6 transcription factor contributes to rice innate immunity through its interaction with Receptor for Activated Kinase-C 1 (RACK1)
1 Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0192, Japan
2 Present address, Universiti Tunku Abdul Rahman Jalan Universiti, Bandar Barat, Kampar, 31900, Malaysia
3 Present address, Department of Advanced Bioscience, Graduate School of Agriculture, Kinki University, 3327-204 Nakamachi, Nara, 631-8505, Japan
Rice 2012, 5:35 doi:10.1186/1939-8433-5-35Published: 11 December 2012
The rice small GTPase OsRac1 is a molecular switch in rice innate immunity. The Receptor for Activated Kinase C-1 (RACK1) interacts with OsRac1 to suppress the growth of the rice blast fungus, Magnaporthe oryzae. RACK1 has two homologs in rice, RACK1A and RACK1B. Overexpressing RACK1A enhances resistance to the rice blast fungus. However, RACK1A downstream signals are largely unknown.
Here, we report the identification of OsRap2.6, a transcription factor that interacts with RACK1A. We found a 94% similarity between the OsRap2.6 AP2 domain and Arabidopsis Rap2.6 (AtRap2.6). Bimolecular fluorescence complementation (BiFC) assays in rice protoplasts using tagged OsRap2.6 and RACK1A with the C-terminal and N-terminal fragments of Venus (Vc/Vn) indicated that OsRap2.6 and RACK1A interacted and localized in the nucleus and the cytoplasm. Moreover, OsRap2.6 and OsMAPK3/6 interacted in the nucleus and the cytoplasm. Expression of defense genes PAL1 and PBZ1 as well as OsRap2.6 was induced after chitin treatment. Disease resistance analysis using OsRap2.6 RNAi and overexpressing (Ox) plants infected with the rice blast fungus indicated that OsRap2.6 RNAi plants were highly susceptible, whereas OsRap2.6 Ox plants had an increased resistance to the compatible blast fungus.
OsRap2.6 contributes to rice innate immunity through its interaction with RACK1A in compatible interactions.