The molecular responses of plants to cold stress have been extensively described, leading to the identification of numerous molecular actors, including a role for Ca 2+-dependent signaling systems. However, the degree to which systemic signaling then integrates the plant’s cold response remains poorly defined. By monitoring the regulation of early cold-responsive genes across Arabidopsis rosettes in response to localized cold stimuli, we confirmed the existence of such systemic signaling. If the plant were simply responding to the lowered ambient temperature, the effect on induction of molecular markers of cold response, such as CRT/DRE BINDING FACTORS 1-3 or MITOGEN ACTIVATED PROTEIN KINASE 6 ( MPK6), might be expected to fall with the distance of the different leaves from the cold source. However, although we observed increased expression in CBF1-3 in the coldest area of the rosette that fell sharply in the leaves further from the stimulus, MPK6 expression was uniformly altered throughout the rosette. This systemic regulation was impaired by application of the Ca 2+-permeable cation channel antagonist La 3+ implying a role for Ca2+ signaling in this response. Using plants expressing GFP-based Ca 2+ biosensors, we show that a localized cold stimulus on a single leaf induces an increase of cytosolic Ca 2+ throughout distal leaves of the plant. Both systemic regulation of early cold responsive genes and propagation of long-distance calcium signals were still observed in the glr3.3/3.6 double mutant that inhibits the propagation of wound-triggered systemic Ca 2+ signals. These observations suggest the existence of a fine-tuned systemic regulation of early cold responsive genes that is driven by a long-distance calcium signaling in a GLR3.3 and GLR3.6 independent manner.