Investigating the mechanism of chloroplast singlet oxygen signaling in the mutant.

As sessile organisms, plants have evolved complex signaling mechanisms to sense stress and acclimate. This includes the use of reactive oxygen species (ROS) generated during dysfunctional photosynthesis to initiate signaling. One such ROS, singlet oxygen (O), can trigger retrograde signaling, chloroplast degradation, and programmed cell death. However, the signaling mechanisms are largely unknown. Several proteins (e.g. PUB4, OXI1, EX1) are proposed to play signaling roles across three mutants that conditionally accumulate chloroplast O ( (), (), and ()). We previously demonstrated that these mutants reveal at least two chloroplast O signaling pathways (represented by and /). Here, we test if the O-accumulating lesion mimic mutant, (), also utilizes these pathways. The allele delayed lesion formation in and restored photosynthetic efficiency and biomass. Conversely, an mutation had no measurable effect on these phenotypes. mutants were not sensitive to excess light (EL) stress, yet and both conferred EL tolerance within the background, suggesting that EL-induced O signaling pathways are independent from spontaneous lesion formation. Thus, O signaling in may represent a third (partially overlapping) pathway to control cellular degradation.