Programmed cell death (PCD) plays critical roles in plant immunity but must be regulated to prevent excessive damage. The E3 ubiquitin ligase SPL11 negatively regulates PCD and immunity in plants. However, the molecular mechanism of SPL11-mediated PCD and immunity is mainly unknown. Recently, researchers at State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection (IPP) of Chinese Academy of Agricultural Sciences (CAAS) have published a research paper about the molecular mechanism of a plasma membrane-resident protein complex consisting of SDS2, SPL11 and OsRLCK118/176modulating PCD and immunity in rice.

SPL11, encoding a plant U-box type E3 ubiquitin ligase, negatively regulates PCD and innate immunity, and the rice spl11 mutant is lesion mimic. They previously isolated three spl11 cell death suppressors (sds1-3). In this study, they reported map-based cloning and characterization of SDS2 that encodes an S-domain RLK. Mutation of SDS2 leads to reduced resistance to the blast fungus Magnaportheoryzae. Conversely, SDS2 over-expression enhances resistance to M. oryzae and induces defense gene expression. They also find that SDS2 interacts with and phosphorylates SPL11, which in turn ubiquitinates SDS2. SDS2 positively regulates rice immunity and interacts with RLCKs OsRLCK118 and OsRLCK176, which are also positive regulators of rice immunity.

Furthermore, OsRLCK118 interacts with and phosphorylates the NADPH oxidase OsRbohB to induce ROS burst during pathogen infection. Taken together, they show that SDS2 is a monocot-specific RLK that plays a positive role in the regulation of PCD and immunity by complexing with the E3 ligase SPL11 and OsRLCK118/176 in rice. More details are available on the bellow links:
http://www.cell.com/cell-host-microbe/fulltext/S1931-3128(18)30100-8