Diatoms play a key role in global phytoplankton productivity and produce a diverse range of valuable terpenoids through two separate pathways: the mevalonate pathway in the cytosol and the methylerythritol phosphate pathway in the plastids. Although recent studies indicate that isoprenoids derived from these pathways are exchanged across intracellular membranes, the transporter proteins facilitating this process remain currently unidentified.</p><p>Here, we employed lovastatin and clomazone to selectively inhibit key enzymes in the MVA and MEP pathways, respectively. We hypothesize that we thereby perturb terpenoid fluxes and force cells to upregulate transmembrane prenyl phosphate transporters. Both inhibitors induced a similar response in diatoms, by significantly reducing cell growth, decreasing photosynthetic efficiency, and lowering terpenoid content clomazone produced a markedly stronger and broader transcriptional response than lovastatin. Notably, clomazone treatment led to widespread downregulation of genes involved in photosynthesis, and chlorophyll biosynthesis.</p><p>We exploited the differential expression analysis for the search for putative prenyl transporters. Our results suggest that members of the ATP binding cassette and major facilitator superfamilies are prime candidates for mediating prenyl phosphate movement across membranes. These findings provide the first set of molecular leads toward elucidating prenyl phosphate transporters in diatoms and lay the groundwork for future functional characterization.