Navigating heavy metal stress: emerging roles of TOR and SnRK signaling in plant tolerance

Abstract

This review explores emerging insights about how plants regulate their responses to heavy metal stress through the coordinated actions of the Target of Rapamycin (TOR) and Sucrose Non-Fermenting-1-Related Kinase (SnRK) signaling pathways. Toxic heavy metals such as As, Pb, Cd and Hg cause severe metabolic and oxidative stress in plants, which reduces their growth and development and ultimately disrupts cellular homeostasis. In this review, we highlight the unique direction of research that focuses on TOR-SnRK interaction under heavy metal exposure, emphasizing their opposite yet interconnected roles in metabolic reprogramming, stress tolerance, and in growth regulation. Under heavy metal stress, SnRK kinases are activated, which triggers the expression of stress-responsive genes and activates autophagy, while downregulating TOR activity to conserve energy and divert resources toward defense, which maintains redox homeostasis, allows plants able to survive. TOR-SnRK pathways interacts with calcium, hormonal, and redox signaling networks, which further strengthen plant stress responses and regulate tolerance mechanisms. Understanding the TOR-SnRK pathway provides a deepened understanding of how plants regulate energy under toxic environmental conditions. In addition to these, targeting these pathways assists in designing crops and agricultural products that are more resilient to heavy metal toxicity, promoting sustainable agriculture in contaminated areas.