Activation of intracellular nucleotide-binding leucine-rich repeat receptors (NLRs) results in immunity and a localized cell death response of infected cells. Cell death activity of many NLRs requires oligomerization and in some cases plasma membrane (PM) localization. However, the exact mechanisms underlying PM localization of NLRs lacking recognizable N- or C-terminal lipidation motifs or predicted transmembrane domains remains elusive. Here we show that the PM localization and stability of members of the RPW8-like coiled-coil (CCR) domain NLRs (RNLs) and a CC-type NLR (CNL) depend on the interaction with PM phospholipids. Depletion of phosphatidylinositol-4-phosphate (PI4P) from the PM led to a mislocalization of the analyzed NLRs and consequently inhibited their cell death activity. We further demonstrate activation-dependent self-association of cell death inducing RNLs. Our results provide new insights into the molecular mechanism of NLR PM localization and defines an important role of phospholipids for CNL and RNL activity during immunity.
34Both type III effector proteins and non-ribosomal peptide toxins play important 35 roles for Pseudomonas syringae pathogenicity in host plants, but whether and how 36 these virulence pathways interact to promote infection remains unclear. Genomic 37 evidence from one clade of P. syringae suggests a tradeoff between the total number of 38 type III effector proteins and presence of syringomycin, syringopeptin, and syringolin A 39 toxins. Here we report the complete genome sequence from P. syringae CC1557, 40 which contains the lowest number of known type III effectors to date and has also 41 acquired genes similar to sequences encoding syringomycin pathways from other 42 strains. We demonstrate that this strain is pathogenic on Nicotiana benthamiana and 43 that both the type III secretion system and a new type III effector family, hopBJ1, 44 contribute to virulence. We further demonstrate that virulence activity of HopBJ1 is 45 dependent on similar catalytic sites as the E. coli CNF1 toxin. Taken together, our 46 results provide additional support for a negative correlation between type III effector 47 repertoires and the potential to produce syringomycin-like toxins while also highlighting 48 how genomic synteny and bioinformatics can be used to identify and characterize novel 49 virulence proteins. 50 51 Introduction 52
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