Salicylate and jasmonate intertwine in ROS-triggered chloroplast-to-nucleus retrograde signaling

Plants, being sessile, are frequently exposed to environmental perturbations, affecting their sustenance and survival. In response, distinct inherent mechanisms emerged during plant evolution to deal with environmental stresses. Among various organelles, chloroplast plays an indispensable role in plant cells. Besides providing the site for photosynthesis and biosynthesis of many important primary and secondary metabolites, including hormones, chloroplasts also act as environmental sensors. Any environmental perturbation directly influences the photosynthetic electron transport chain, leading to excess accumulation of reactive oxygen species (ROS), causing oxidative damages to biomolecules in the vicinity. To prevent excess ROS accumulation and the consequent oxidative damages, the chloroplast activates retrograde signaling (RS) pathways to reprogramme nuclear gene expression, defining plant's response to stress. Based on levels and site of ROS accumulation, distinct biomolecules are oxidized, generating specific derivatives that act as genuine signaling molecules, triggering specific RS pathways to instigate distinctive responses, including growth inhibition, acclimation, and programmed cell death. Though various RS pathways independently modulate nuclear gene expression, they also implicate the defense hormone salicylic acid (SA) and oxylipins, including 12-oxo-phytodienoic acid (OPDA) and jasmonic acid (JA), by promoting their biosynthesis and utilizing them for intra- and intercellular communications. Several studies reported the involvement of both hormones in individual RS pathways, but the precise dissection of their activation and participation in a given RS pathway remains an enigma. The present review describes the current understanding of how SA and JA intertwine in ROS-triggered RS pathways. We have also emphasized the future perspectives for elucidating stress specificity and spatiotemporal accumulation of respective hormones in a given RS pathway.