Abstract
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 ((1)O(2)), 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 Arabidopsis thaliana mutants that conditionally accumulate chloroplast (1)O(2) (fluorescent in blue light (flu), chlorina 1 (ch1), and plastid ferrochelatase 2 (fc2)). We previously demonstrated that these mutants reveal at least two chloroplast (1)O(2) signaling pathways (represented by flu and fc2/ch1). Here, we test if the (1)O(2)-accumulating lesion mimic mutant, accelerated cell death 2 (acd2), also utilizes these pathways. The pub4-6 allele delayed lesion formation in acd2 and restored photosynthetic efficiency and biomass. Conversely, an oxi1 mutation had no measurable effect on these phenotypes. acd2 mutants were not sensitive to excess light (EL) stress, yet pub4-6 and oxi1 both conferred EL tolerance within the acd2 background, suggesting that EL-induced (1)O(2) signaling pathways are independent from spontaneous lesion formation. Thus, (1)O(2) signaling in acd2 may represent a third (partially overlapping) pathway to control cellular degradation.