Centrosomes are required for efficient cell cycle progression mainly by orchestrating microtubule dynamics and facilitating G1/S and G2/M transitions. However, the role of centrosomes in S-phase progression is largely unknown. Here, we report that depletion of FOR20 (FOP-related protein of 20 kDa), a conserved centrosomal protein, inhibits S-phase progression and prevents targeting of Plk1 (polo-like kinase 1) to centrosomes, where FOR20 interacts with Plk1. Ablation of Plk1 also significantly induces S-phase defects, which are reversed by ectopic expression of Plk1, even a kinase-dead mutant, but not a mutant that fails to localize to centrosomes. Exogenous expression of centrosome-tethered Plk1, but not wild-type Plk1, overrides FOR20 depletion-induced S-phase defects independently of its kinase activity. Thus, these data indicate that recruitment of Plk1 to centrosomes by FOR20 may act as a signal to license efficient progression of S-phase. This represents a hitherto uncharacterized role of centrosomes in cell cycle regulation.