Ascorbic acid: a metabolite switch for designing stress-smart crops.

Plant growth and productivity are continually being challenged by a diverse array of abiotic stresses, including: water scarcity, extreme temperatures, heavy metal exposure, and soil salinity. A common theme in these stresses is the overproduction of reactive oxygen species (ROS), which disrupts cellular redox homeostasis causing oxidative damage. Ascorbic acid (AsA), commonly known as vitamin C, is an essential nutrient for humans, and also plays a crucial role in the plant kingdom. AsA is synthesized by plants through the d-mannose/l-galactose pathway that functions as a powerful antioxidant and protects plant cells from ROS generated during photosynthesis. AsA controls several key physiological processes, including: photosynthesis, respiration, and carbohydrate metabolism, either by acting as a co-factor for metabolic enzymes or by regulating cellular redox-status. AsA's multi-functionality uniquely positions it to integrate and recalibrate redox-responsive transcriptional/metabolic circuits and essential biological processes, in accordance to developmental and environmental cues. In recognition of this, we present a systematic overview of current evidence highlighting AsA as a central metabolite-switch in plants. Further, a comprehensive overview of genetic manipulation of genes involved in AsA metabolism has been provided along with the bottlenecks and future research directions, that could serve as a framework for designing "stress-smart" crops in future.

Loss of Myo19 increases metastasis by enhancing microenvironmental ROS gradient and chemotaxis.

Tumor metastasis involves cells migrating directionally in response to external chemical signals. Reactive oxygen species (ROS) in the form of H2O2 has been demonstrated as a chemoattractant for neutrophils but its spatial characteristics in tumor microenvironment and potential role in tumor cell dissemination remain unknown. Here we investigate the spatial ROS distribution in 3D tumor spheroids and identify a ROS concentration gradient in spheroid periphery, which projects into a H2O2 gradient in tumor microenvironment. We further reveal the role of H2O2 gradient to induce chemotaxis of tumor cells by activating Src and subsequently inhibiting RhoA. Finally, we observe that the absence of mitochondria cristae remodeling proteins including the mitochondria-localized actin motor Myosin 19 (Myo19) enhances ROS gradient and promotes tumor dissemination. Myo19 downregulation is seen in many tumors, and Myo19 expression is negatively associated with tumor metastasis in vivo. Together, our study reveals the chemoattractant role of tumor microenvironmental ROS and implies the potential impact of mitochondria cristae disorganization on tumor invasion and metastasis.