Evidence is presented to suggest that several early events of zoospore germination in the water mold, Blastocladiella emersonii, are not dependent upon concomitant protein synthesis. The events involve abrupt, dramatic changes in cell architecture. On account of this evidence, as well as evidence available from other sources, we question whether differential protein synthesis provides an exclusive and sufficient mechanism for phenotypic change (i.e., cell differentiation). Rather, we argue that mechanisms for bringing about structural alterations in the preformed machinery of the cell should also be given attention.One common thread runs through virtually all current thinking regarding the mechanism(s) of cellular differentiationnamely, that cells change phenotype (i.e., differentiate) as a result of differential protein synthesis. Our intention in this paper is certainly not to discredit the usefulness of this hypothesis, but rather to call into question whether this form of phenotypic control provides an exclusive and sufficient mechanism for cellular differentiation.The organism under study is the water mold Blastocladiella emersonii. We have focused attention particularly on the sequence of cellular changes involved in zoospore germination, primarily because this sequence is characterized by dramatic, abrupt changes in cell structure, and because zoospore populations can be induced to germinate rapidly and semisynchronously (1). A sequence of four morphologically distinct cell types can be unambiguously resolved (see Fig. 1 and refs.