Investigating the mechanism of chloroplast singlet oxygen signaling in theArabidopsis thaliana accelerated cell death 2mutant

Abstract

AbstractAs 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 (1O2), 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 threeArabidopsis thalianamutants that conditionally accumulate chloroplast1O2(fluorescent in blue light(flu),chlorina 1(ch1), andplastid ferrochelatase 2(fc2)). We previously demonstrated that these mutants reveal at least two chloroplast1O2signaling pathways (represented byfluandfc2/ch1). Here, we test if the1O2-accumulating lesion mimic mutant,accelerated cell death 2(acd2), also utilizes these pathways. Thepub4-6allele delayed lesion formation inacd2and restored photosynthetic efficiency and biomass. Conversely, anoxi1mutation had no measurable effect on these phenotypes.acd2mutants were not sensitive to excess light (EL) stress, yetpub4-6andoxi1both conferred EL tolerance within theacd2background, suggesting that EL-induced1O2signaling pathways are independent from spontaneous lesion formation. Thus,1O2signaling inacd2may represent a third (partially overlapping) pathway to control cellular degradation.