The breaking of dormancy in seeds can be elicited by many factors, including temperature and short exposure to low molecular weight amphipathic molecules such as primary alcohols, monocarboxylic acids and anaesthetics. Their action has been suggested to be mediated through effecting changes to membranes. Paradoxically, though, these molecules can inhibit the germination of some non-dormant seeds. Here, we review the structure–activity relationships between amphipathic molecules and dormancy breaking and, based on the known responses of membranes to them and to temperature changes, offer an alternative interpretation of the data and a new hypothesis to explain their action. We suggest that amphipathic molecules break dormancy by partitioning into the membrane, thereby increasing and optimizing phospholipid headgroup spacing. This, in turn, facilitates the binding and activation of a peripheral membrane protein component of a signal transduction pathway that is essential for the completion of germination. In cases where amphipathic molecules inhibit germination, it is predicted that they cause the optimal headgroup spacing to be exceeded, thus preventing subsequent association of the membrane with the peripheral protein component. The hypothesis is extended to explain membrane changes that can lead to dormancy breaking during dry after-ripening.