The Monocot-Specific Receptor-like Kinase SDS2 Controls Cell Death and Immunity in Rice

Abstract

SUMMARY 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. We show that SPL11 cell-death suppressor 2 (SDS2), an S-domain receptor-like kinase, positively regulates PCD and immunity in rice by engaging and regulating SPL11 and related kinases controlling defense responses. An sds2 mutant shows reduced immune responses and enhanced susceptibility to the blast fungus Magnaporthe oryzae. Conversely, SDS2 over-expression induces constitutive PCD accompanied by elevated immune responses and enhanced resistance to M. oryzae. SDS2 interacts with and phosphorylates SPL11, which in turn ubiquitinates SDS2, leading to its degradation. In addition, SDS2 interacts with related receptor-like cytoplasmic kinases, OsRLCK118/176, that positively regulate immunity by phosphorylating the NADPH oxidase OsRbohB to stimulate ROS production. Thus, a plasma membrane-resident protein complex consisting of SDS2, SPL11, and OsRLCK118/176 controls PCD and immunity in rice.

A cyclic nucleotide-gated channel mediates cytoplasmic calcium elevation and disease resistance in rice

“…43 It is worth mentioning that besides OsRLCK185, several other OsRLCKs have been shown to be involved in regulation of PTI responses and disease resistance in rice. 9,18 Their regulatory relationship with OsCERK1 and OsCNGC9 will be an interesting avenue for future research. In addition, there is also evidence suggesting that the activation of MAPK cascades and anion channel opening are also triggered by pattern recognition.…”

“…15,16 On the other hand, accumulating evidence indicates PTI-mediated blast resistance also operates in rice. [17][18][19] However, the signaling mechanisms governing PTI-mediated blast resistance in rice remain poorly understood.…”

The Catalase Gene Family in Cotton: Genome-Wide Characterization and Bioinformatics Analysis

“…Recent several studies have revealed that ROS are essential for maintaining normal cellular functions, as opposed to having a toxic effect on cells [2]. Even cell death that was previously considered a result from oxidative damage is now thought to be a ROS-mediated physiological pathway for programmed cell death, rather than directly killing the cells [3,4]. Additionally, ROS levels that are too low are cytostatic for cells, whereas ROS levels that are too high are cytotoxic [5].…”

Post-Translational Modifications of Proteins Have Versatile Roles in Regulating Plant Immune Responses

“…Several RLCK VII members are immediate downstream signaling components of OsCERK1, including OsRLCK57, OsRLCK185, OSRLCK107, OsRLCK118 and OsRLCK176. OsRLCK118, OsRLCK176, and OsRLCK185 also emerged as substrates of other PRRs, including lysin motif-containing protein (LYP4), LYP6, and SPL11 cell-death suppressor2 [55,76], suggesting that the phosphorylation signaling triggered by PAMPs is transduced from PRRs located on the cell surface to cell cytoplasmic proteins dependent on these RLCKs.…”