Figure 7. Model for immune receptor-mediated recognition of pathogen and resultant defense gene activation.

In uninfected cells, nuclear N does not associate with SPL6; as a result defense genes are not transcribed. Following TMV infection, there are 3 distinct phases for successful activation of a defense response. In phase I (Effector association), the viral effector promotes the relocalization of chloroplast NRIP1 into the cytoplasm and the p50-U1 and NRIP1 complex associates with N. This ternary complex could, by an as yet unknown mechanism, promote an ATP-dependent conformational change in N potentiating it for further signaling events. The N^GK221-222AA P-loop mutant can associate with p50-U1 but is unable to undergo the conformational change and hence is not activated. p50-Ob from the non-eliciting TMV-Ob strain can also associate with N, but may not be able to induce a conformational change. Phase II (Activation) - The ATP bound N may associate with nuclear SPL6 (pathway A) thereby activating defense gene expression. Alternately, N undergoes TIR domain-mediated oligomerization leading to recruitment of unknown host protein(s) that activate(s) N. This oligomerized N complex may associate with nuclear SPL6 (pathway B). In phase III (transcriptional regulation), activated N associates with SPL6. This either enhances SPL6 interaction with the specific defense responsive gene promoters or leads to recruitment of transcription machinery. The end result is the transcription of key immune response genes whose products are required for efficient induction of HR-PCD and defense.