Following tuber induction, potato tubers undergo a period of dormancy during which visible bud growth is inhibited. The length of the dormancy period is under environmental, physiological and hormonal control. Sucrose availability is one prerequisite for bud break. In the absence of sucrose, no bud break occurs. Thus, sucrose is likely to serve as nutrient and signal molecule at the same time. The mode of sucrose sensing is only vaguely understood, but most likely involves trehalose-6-phosphate and SnRK1 signalling networks. This conclusion is supported by the observation that ectopically manipulation of trehalose-6-phosphate levels influences the length of the dormancy period. Once physiological competence is achieved, sprouting is controlled by the level of phytohormones. Two phytohormones, ABA and ethylene, are supposed to suppress tuber sprouting; however, the exact role of ethylene remains to be elucidated. Cytokinins and gibberellins are required for bud break and sprout growth, respectively. The fifth classical phytohormone, auxin, seems to play a role in vascular development. During the dormancy period, buds are symplastically isolated, which changes during bud break. In parallel to the establishment of symplastic connectivity, vascular tissue develops below the growing bud most likely to support the outgrowing sprout with assimilates mobilised in parenchyma cells. Sprouting leads to major quality losses of stored potato tubers. Therefore, control of tuber sprouting is a major objective in potato breeding. Although comparative transcriptome analysis revealed a large number of genes differentially expressed in growing versus dormant buds, no master-regulator of potato tuber sprouting has been identified so far.