PRRs (usually a protein complex with at least one protein with a protein kinase domain) activate a series of intracellular protein kinases (PK), which can activate transcription factors (TF). Some of the PKs activate NADPH oxidases that produce ROS and also activate calcium channels that promote additional signaling. Pathogen effectors can interfere with function of PRRs or other PKs, with other host components (not shown) and also with TFs. These effectors can be detected (indicated by red arrows) either directly or indirectly by CNLs or TNLs, resulting in NLR oligomerization. TNL oligomerization to a tetramer creates an NADase enzyme activity that produces small molecules that activate EDS1 family proteins to engage with RNLs enabling RNL oligomerization (the structure of RNL oligomers, depicted here as a tetramer, is as yet unknown). RNL interactions with EDS1 family proteins can also activate transcription. CNL and RNL oligomerization lead directly to the generation of plasma membrane channels. Thus, NLR activation and oligomerization culminate by diverse paths in creation of calcium channels that promote immune activation. To avoid extra complexity in the cartoon, the mutual potentiation mechanisms between surface- and intracellular-receptor initiated signaling are not shown.
