The phenylpropanoid pathway is big in plants-particularly in trees, which can get big in no small part because of the lignin produced through this pathway. In addition to the huge carbon sink represented by lignin (reviewed in Eudes et al., 2014), the phenylpropanoid pathway also produces important small molecules such as flavonoids. By contrast, the glucosinolate pathway is small potatoes-or rather, small Brussels sprouts, as these sulfur-and nitrogen-containing compounds generally occur in Brassica species, including Arabidopsis thaliana (reviewed in Baskar et al., 2012). Glucosinolates participate in plant defenses against herbivores and occur in broadly varying types; for example, Arabidopsis Col-0 produces ;30 different glucosinolates. Different glucosinolates form from different precursor amino acids, including Trp (indole glucosinolates), Ala, Ile, Leu, Met, or Val (aliphatic glucosinolates), and Phe or Tyr (aromatic glucosinolates).To examine secondary metabolism, Kim et al. (2015) characterize the reduced epidermal fluorescence5 (ref5) mutant, which has reduced levels of phenylpropanoids, resulting in decreased fluorescence under UV light (see figure). Positional cloning showed that REF5 encodes the cytochrome P450 monooxygenase CYP83B1, an enzyme involved in biosynthesis of indole glucosinolates. Indeed, although ref5 was originally identified by its reduced levels of the phenylpropanoid compound sinapoylmalate, the ref5 mutant also has reduced levels of indole glucosinolates. Moreover, accumulation of the glucosinolate precursor indole-3-acetaldoxime (IAOx) results in increased production of indole-3-acetic acid, causing high-auxin phenotypes, such as longer hypocotyls, in the ref5 mutants.In addition to high-auxin phenotypes, IAOx accumulation changes phenylpropanoid metabolism. The authors showed this by examining triple mutants affecting CYP831B and the upstream enzymes CYP79B2 and CYP79B3, which produce IAOx. They found that the triple mutants do not accumulate IAOx and also show higher levels of sinapoylmalate, indicating that the low-sinapoylmalate phenotype results from high IAOx, not low indole glucosinolates. Examination of phenylalanine, flavonoids, and other intermediates in the phenylpropanoid pathway in different mutants also showed that the inhibitory effect of IAOx likely occurs early in the pathway, possibly acting on the first committed enzyme of the pathway, PHENYL-ALANINE AMMONIA LYASE2. Double mutants of REF5 and CYP83A1/REF2, which encodes another enzyme in the glucosinolate pathway, showed a synergistic effect on the phenylpropanoid pathway, with a 96% reduction in sinapoylmalate contents compared with a 70% reduction in each single mutant. Moreover, a screen for suppressors of ref5 identified a subunit of the Mediator complex, indicating that changes in transcription involving the Mediator complex may cause the repression of the phenylpropanoid pathway.Identification of the crosstalk between glucosinolate and the phenylpropanoid pathway, and of the role of the Mediator complex, ...