@article {Yu641241, author = {Gang Yu and Liu Xian and Hao Xue and Wenjia Yu and Jose Rufian and Yuying Sang and Rafael Morcillo and Yaru Wang and Alberto P. Macho}, title = {A bacterial effector protein prevents MAPK-mediated phosphorylation of SGT1 to suppress plant immunity}, elocation-id = {641241}, year = {2019}, doi = {10.1101/641241}, publisher = {Cold Spring Harbor Laboratory}, abstract = {Nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as sensors that perceive pathogen molecules and activate immunity. In plants, the accumulation and activation of NLRs is regulated by SUPPRESSOR OF G2 ALLELE OF skp1 (SGT1). In this work, we found that the plant pathogen Ralstonia solanacearum secretes an effector protein, named RipAC, inside plant cells, and it associates with SGT1 to suppress NLR-mediated SGT1-dependent immune responses. RipAC does not affect the accumulation of SGT1, NLRs, or their interaction. However, RipAC inhibits the interaction between SGT1 and MAP kinases, and the phosphorylation of a MAPK target motif in the C-terminal domain of SGT1, which is required for the interaction with NLRs. Such phosphorylation releases the interaction between SGT1 and the NLR RPS2, and contributes to the activation of RPS2-mediated responses. Our results shed light onto the mechanism of activation of NLR-mediated immunity, and suggest a positive feedback loop between MAPK activation and SGT1-dependent NLR activation.Significance Statement The activation of immune receptors that perceive pathogen molecules and initiate immune signaling is tightly regulated. In plants and animals, SGT1 is a major regulator of the accumulation and activation of such receptors, although the mechanisms of this regulation are not well understood. In this work, we found that the plant pathogenic bacteria Ralstonia solanacearum, causal agent of the bacterial wilt disease, secretes an effector protein inside plant cells that suppresses the phosphorylation-dependent activation of SGT1, which in turn inhibits the activation of SGT1-dependent immune receptors. These findings provide new insights into a general mechanism of regulation of immunity, and uncover a new virulence strategy employed by a bacterial pathogen to contribute to disease development.}, URL = {https://www.biorxiv.org/content/early/2019/09/25/641241}, eprint = {https://www.biorxiv.org/content/early/2019/09/25/641241.full.pdf}, journal = {bioRxiv} }