The social amoeba Polysphondylium violaceum uses chemoattractants different from those of Dictyoctelium discoideum for cell aggregation. However, the detailed mechanisms in P. violaceum remain unknown. We have previously reported that the polyketide synthase StlA is involved in inducing aggregation in this species. To elucidate the mechanism of StlA-induced aggregation in P. violaceum, we analysed the phenotype of Pv-stlA- mutants in more detail. Unlike our previous results, the mutant cells did not exhibit proper chemotaxis towards glorin. Defective aggregation was not restored by glorin pulses, 8Br-cAMP, or deletion of the homologue of PufA that is a translational repressor of PKA, whereas mutant cells grown in the presence of 4-methyl-5-pentylbenzene-1,3-diol (MPBD), the putative Pv-StlA product, aggregated normally without it after starvation. Furthermore, the early developmental marker gene, dscA, was down-regulated in the mutant cells. Our data thus suggested that StlA is required for the transition from growth to development in P. violaceum.