Early embryogenesis is characterized by rapid and synchronous cleavage divisions, which are often controlled by wave-like patterns of Cdk1 activity. Two mechanisms have been proposed for mitotic waves: sweep and trigger waves 1,2. The two mechanisms give rise to different wave speeds, dependencies on physical and molecular parameters, and spatial profiles of Cdk1 activity: upward sweeping gradients vs traveling wavefronts. Both mechanisms hinge on the (transient) bistability of the potential that appears in the reactiondiffusion dynamics governing the progression of the cell cycles across the embryo. The two types of waves are differentiated by the speed of the cell-cycle progression: Sweep/trigger waves arise for rapid/slow drives, respectively. Here, using quantitative imaging of Cdk1 activity and theory, we first illustrate that sweep waves are the dominant mechanism in Drosophila embryos, and then test two fundamental predictions on the transition from sweep to trigger waves. Specifically, we demonstrate that sweep waves can be turned into trigger waves if the cell cycle is slowed down genetically or if significant delays in the cell cycle progression are introduced across the embryo by altering nuclear density. Our genetic experiments demonstrate that Polo kinase is a major rate-limiting regulator of the timing of blastoderm divisions and is highly effective at inducing the sweep to trigger transitions. Furthermore, we test the effects of temperature on cell cycle timing and mitotic waves. We show that changes in temperature cause an essentially uniform slowdown of interphase and mitosis. That results in sweep waves still being observed across a wide temperature range in spite of the cell cycle durations being significantly longer. Collectively, our combination of theory and quantitative imaging elucidates the nature of mitotic waves in Drosophila embryogenesis, their control mechanisms and their mutual transitions.