Figure 3
Comparison of CaMV and TuMV transmission activation. The left part of the schematized cell (not drawn to scale) presents a TuMV-infected and the right part a CaMV-infected cell (adapted from7). (A) Before aphid arrival, infected cells are in an unstressed standby stage and the cytoplasmic redox potential has normal reducing values (light green color of the cytoplasm). TuMV virions and HC-Pro are distributed evenly throughout the cytoplasm but cannot interact because HC-Pro is in its reduced conformation (-SH). CaMV virions are contained in virus factories and P2, together with P3, in transmission bodies. Thus, no or only few transmissible complexes are present. (B) Alighting aphids test plants by brief stylet punctures in leaf cells and inject saliva into the cytoplasm before aspiring some cell contents. Presumably, a saliva component or a DAMP binds to corresponding PRR(s) and triggers calcium and ROS signaling. Downstream events will eventually install plant defenses in a classical PTI reaction. The initial calcium waves and the accompanying ROS production change the redox potential of the cytoplasm to increasingly oxidized values (green cytoplasm). HC-Pro becomes oxidized and forms oligomers via intermolecular sulfur bridges (S-S). For CaMV, the calcium signal and the redox change induce entry of tubulin in transmission bodies. The calcium channel blocker LaCl3 inhibits calcium signaling, and applying H2O2 mimics ROS generation, thus explaining their effects on TA. (C) When the cytoplasm is maximally oxidized (dark green cytoplasm) HC-Pro oligomers bind to TuMV virions to form TuMV transmissible complexes. The inhibitory action of NEM on TuMV transmission could be by inhibiting HC-Pro oligomerization. For CaMV, the oxidizing conditions induce dissociation of the transmission bodies. Free P2 binds to microtubules and virions, dispatched from the virus factories, join P2 and form CaMV transmissible complexes. Now TuMV and CaMV infected cells are in the transmission-activated stage and vectors acquire and transmit virus efficiently. How azide inhibits TuMV and boosts CaMV transmission, is unclear. TA of TuMV but not of CaMV might propagate in the tissue. (D) After aphid departure, the cytoplasmic redox potential returns to reducing values, TuMV and CaMV transmissible complexes dissociate and the cells return to the standby stage.
