Abstract text: Hormesis is a biphasic dose–response relationship in which low levels of a stressor stimulate growth, while higher doses cause toxicity. Cadmium (Cd) is widely recognized as a toxic heavy metal; at low concentrations, it can trigger beneficial responses. Despite growing evidence, the mechanistic understanding of Cd-induced hormesis remains elusive. The plant cell wall is a static barrier, with a dynamic matrix whose mechanical properties are largely determined by the organization of pectin, cellulose, and hemicellulose, which continuously adjusts in response to developmental and environmental cues. In particular, the methylesterification status of homogalacturonan (HG), regulated by pectin methylesterases (PMEs), determines Ca²⁺-mediated cross-linking and wall plasticity. Notably, PME activity releases methanol as a by-product of pectin demethylesterification, which may induce methanol-responsive pathways and could be associated with changes in photosynthetic efficiency and plant growth.

Low-dose Cd exposure enhances root and shoot growth, biomass accumulation, and photosynthetic efficiency, while reducing stress markers. Molecular and biochemical analyses revealed coordinated pectin remodelling, balanced Ca²⁺ reinforcement, and tightly regulated methanol production under hormetic conditions. Our data suggest that Cd-induced hormesis operates through coordinated cell wall remodelling and methanol-associated responses, which together optimize structural plasticity and photosynthetic performances.