The growth rates of BY4741 and AD1-9 in the presence of all compounds tested are depicted in Figure S1. As expected, growth of the drug-efflux pump deficient strain was more often and more strongly inhibited than that of the wild-type strain. Altogether, 231 compounds inhibited growth of BY4741 and/or AD1-9. To identify meiosis-specific inhibitors, all drugs in the NCC were subsequently interrogated with the two sporulation assays. For these experiments we used the efficiently-sporulating SK1 strain background, which was not deficient in any of the drugefflux pumps. Similar to the growth data, we calculated sensitivity scores for every compound. This score indicates how strongly a compound inhibited sporulation in the assay compared to the “no drug” controls. To minimize false positives and prioritize secondary experiments, a highly stringent cutoff was applied. A scatterplot depicts the sensitivity scores ABT-263 determined this wayand a Venn diagram summarizes the overlap of compounds identified in the three different screening approaches. In summary, 200 drugs had no effect in any of the assays; 231 inhibited growth and 64 inhibited sporulation. 49 drugs inhibited vegetative growth and sporulation. All sensitivity scores are listed in Table S1. 15 compounds were found to specifically inhibit spore formation. We re-tested these chemicals in sporulating cultures and determined the percentage of spores after 48 hours. Note that these experiments were performed in small liquid cultures, which are sub-optimally aerated, and thus only intermediate sporulation efficiencies were observed. Nevertheless, 10 of the 15 compounds completely abolished spore formation and 2 chemicalshad moderate inhibitory effects. The remaining 3 compounds were indistinguishable from the control and were not further analyzed. Taken together, the Talazoparib 1207456-01-6 confirmation rate was 80%. Five of the twelve compoundswere identified in the sporulation assay only. Another set of 5 drugswas identified in the recombination assay only. The remaining 2 compoundswere identified in both assays. We noticed a similarity in molecular structures among the inhibitory compounds: all contained a hydrophobic ring system and a basic nitrogen-containing group, which are the attributes of a class of compounds called cationic amphiphilic drugs. The primary targets of these drugs in man are monoamine receptors, and many are widely used anti-depressants and antipsychotics. These drugs are not only known to interact with their protein targets, but also with phospholipid membranes. Yeast lack proteins with sequence similarity to monoamine receptors, therefore, these drugs likely repress sporulation by inhibiting alternative proteins or cellular components. We chose tripelennamineas a representative for this class of compounds, and studied its effect on yeast sporulation in more detail. We first determined sporulation efficiency in the presence of TA in largeliquid cultures. As expected the “no drug” control yielded,95% mature spores within the first 24 hours, and ammonium sulfate strongly reduced spore formation to only about 10% after 3 days. In contrast, TA completely abolished sporulation at a concentration of 100 mM. Even after 72 hours no spores were detected in the TA-treated culture. Upon visual inspection of sporulating cultures by microscopy, marked morphological differences were observed in these three conditions. In the “no 
drug” control, most cells had formed an ascus with spores, whereas the ammonium sulfate-treated cells had round and inflated shapes. In contrast, cells that were sporulated in the presence of TA had accumulated small granular bodies of unknown nature, but were devoid of spores.