FIG. 7.

Putative model for symptom modulation by TCV subviral RNAs in Arabidopsis. In this model, the TCV CP (indicated by small gray circles) binds directly to the 3′ ends of satC and diG and competes for binding with a putative host factor, X (indicated by large black circles), that is involved in virus long-distance movement. I, symptom intensification; R, resistance (i.e., symptom attenuation); U, unaffected symptoms. (A) When high levels of CP are present, CP outcompetes X for binding to the 3′-terminal stem-loops of both satC and diG, leaving X available for virus long-distance movement (i.e., systemic infection). (B) When low levels of CP are present, X outcompetes the CP for binding to the 3′-terminal stem-loop of satC but not that of diG, and sequestration of X by satC restricts virus movement and results in symptom attenuation. In contrast, CP outcompetes X for binding to the 3′-terminal stem-loop of diG, due to the higher affinity of the diG-like hairpin for binding to CP. Why symptoms are not intensified under these conditions is not known. (C) X outcompetes non-TCV CP such as CCFV CP (indicated by small brick-patterned circles) for binding to the 3′ ends of both satC and diG, and sequestration of X by the subviral RNAs restricts virus movement and results in symptom attenuation. Note that satC and diG are more abundant in the absence of TCV CP than in the presence of TCV CP as previously found (16).