In the absence of infection (left), RLD function, which partially depends on its interaction with and recruitment by LZY proteins, contributes to normal plant development. When TYLCV infects the cell (middle), its C4 protein interacts with RLD proteins and recruits them to the plasma membrane (PM), to which it is associated by myristoylation. C4 outcompetes LZY proteins, and potentially other endogenous interactors of RLD proteins, for RLD binding; this results in the disruption of RLD function and the concomitant alterations of development that are recognized as viral symptoms, which ultimately act as attractants for the whitefly insect vector. This higher whitefly attraction to virus-infected plants may favor acquisition and vector transmission of TYLCV. If plants are artificially inoculated with a mutant virus producing a CCL-like-domain-deficient version of C4 (TYLCVC4CCLm3) (right), the interaction with RLDs is abolished, so RLD function is maintained and plant development is not affected, rendering infected plants symptomless and reducing attractiveness to whiteflies. Of note, viral accumulation is not significantly affected by the lack of a CCL-like domain in C4, indicating that symptom development and viral performance in the plant host can be uncoupled.
