Control of organelle size and volume is important to ensure appropriate membrane tension and concentration of soluble contents. Under steady-state conditions, the size of membrane-enclosed organelles scales with cell size, but during cell growth, organelles expand without bursting by adjusting the volume of the boundary membrane to the amount of content. Although the molecular basis of these adjustments is not fully understood, fusion or fission events have been implicated. Andreas Mayer and colleagues study fusion of yeast vacuoles and have previously shown that the vacuolar transporter chaperone (VTC) complex is necessary for the process. VTC has since been described as the major polyphosphate (polyP) polymerase in yeast and, because polyP is the main component of yeast vacuoles, the authors now ask (p. 2817) whether VTC can stimulate vacuole fusion by changing the abundance of vacuole content. Indeed, they show here that accumulation of polyP inside vacuoles controls vacuolar fusion, whereas increased cytoplasmic amounts did not have an effect. Mechanistically, accumulation of polyP promotes recruitment of the chaperone Sec18 (also known as N-ethylmaleimide-sensitive factor, NSF) to vacuolar SNAREs, which activates them and so triggers fusion. This also implicates activity of the cyclin-dependent kinase Pho80–Pho85. Taken together, these findings support a model whereby increased luminal load controls homotypic vacuolar fusion to augment storage space, while maintaining an appropriate volume-to-surface ratio.