Fig. 1.

Proposed interactions between RNA editing and chloroplast signaling. In well-functioning photosynthetic cells (Left), chlorophyll accumulates in the thylakoid membranes (green), and chloroplasts perform photosynthesis. The GUN1 protein does not accumulate and thus the chloroplast-to-nucleus signaling that depends on GUN1 is not active. MORF2 contributes to RNA editing (green arrow) and interacts with OPT81, OPT84, and YS1. Light signaling, tissue-specific signals, and the circadian rhythm (not shown) drive high-level expression of PhANGs (black arrow), which promotes chloroplast function. Blocking chloroplast biogenesis at a stage resembling the proplastid leads to the development of dysfunctional photosynthetic cells (Right) containing dysfunctional chloroplasts that do not accumulate chlorophyll or perform photosynthesis. In these cells, GUN1 accumulates and regulates RNA editing by interacting with MORF2 (red arrow). Abnormal RNA editing activates a chloroplast-to-nucleus signaling mechanism that down-regulates PhANG expression (red T-bar). Similarly, GUN1 accumulates during the early stages of leaf development—before chloroplast biogenesis is completed (11)—and regulates RNA editing and chloroplast-to-nucleus signaling as it does in dysfunctional photosynthetic cells.