The Receptor-like Kinase SDS2 Complexes with the E3 Ligase SPL11 and Two Receptor-Like Cytoplasmic Kinases to Regulate Cell Death and Immunity in Rice
J. FAN (1), G. Wang (1) (1) Department of Plant Pathology, The Ohio State University, U.S.A.

Programmed cell death (PCD) plays a critical role in plant innate immunity against pathogens. However, the mechanism underline PCD is not fully understood. We previously reported that the U-box E3 ligase SPL11/PUB13 is a negative regulator of PCD and innate immunity in plants. Here, we show that SDS2 (Spl11 Cell-Death Suppresor2) positively regulates PCD and innate immunity in rice. sds2 mutant plants show enhanced susceptibility to the rice blast fungus Magnaporthe oryzae and reduced ROS generation after the PAMP flg22, chitin or LPS treatments. Conversely, over-expression of SDS2 in rice leads to the formation of cell death lesions, elevated PR gene expression, enhanced resistance to M. oryzae and elevated ROS production upon PAMP treatments. SDS2 encodes an S-domain type receptor-like kinase. The protein interacts with, and phosphorylates SPL11 and is degraded by the latter in a kinase-activity dependent manner. Interestingly, SDS2 interacts with two receptor-like cytoplasmic kinases, SDRK1 and SDRK2. SDS2 and SDRK2 transphosphorylate each other. Both sdrk1 and sdrk2 mutants show reduced resistance to M. oryzae and reduced ROS production after PAMP treatments. In addition, the Sdrk2 mutation suppresses spl11-mediated cell death. These results demonstrate that a multiple protein complex consisting of the receptor-like kinase SDS2, the E3 ligase SPL11 and receptor-like cytoplasmic kinases SDRK1 and SDRK2 controls PCD and innate immunity in rice. 

Abstract Number: P18-667
Session Type: Poster