We treat the diatom Phaeodactylum tricornutum with Clomazone and Lovastatin and perform RNA-seq to identify putative prenyl phosphate transporters

Diatoms play a key role in global phytoplankton productivity and produce a diverse range of valuable terpenoids through two separate pathways: the mevalonate (MVA) pathway in the cytosol and the methylerythritol phosphate (MEP) 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. Here, we employed lovastatin and clomazone to selectively inhibit 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 showed a similar phenotype, by significantly reducinged cell growth, diminished diminishing photosynthetic efficiency, and lowered lowering terpenoid content; clomazone produced a markedly stronger and broader transcriptomic response than lovastatin. Notably, clomazone treatment led to widespread downregulation of genes involved in photosynthesis, and chlorophyll biosynthesis. Additionally, also the MEP pathway was downregulated, which is the opposite regulatory response that has been observed in other organisms. Differential expression analysis for the discovery of putative prenyl transporters focused predominantly on members of the ATP-binding cassette (ABC) and major facilitator superfamilies (MFS) as 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.