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SUMMARY Meristem function is underpinned by numerous genes that affect hormone levels, ultimately controlling phyllotaxy, the transition to flowering and general growth properties. Class I KNOX genes are major contributors to this process, promoting cytokinin biosynthesis but repressing gibberellin production to condition a replication competent state. We identified a suppressor mutant of theKNOX1mutantbrevipedicellus(bp) that we termedflasher(fsh), which promotes stem and pedicel elongation, suppresses early senescence, and negatively affects reproductive development. Map‐based cloning and complementation tests revealed thatfshis due to an E40K change in the flavin monooxygenaseGS‐OX5, a gene encoding a glucosinolate (GSL) modifying enzyme.In vitroenzymatic assays revealed thatfshpoorly converts substrate to product, yet the levels of several GSLs are higher in the suppressor line, implicatingFSHin feedback control of GSL flux.FSHis expressed predominantly in the vasculature in patterns that do not significantly overlap those ofBP, implying a non‐cell autonomous mode of meristem control via one or more GSL metabolites. Hormone analyses revealed that cytokinin levels are low inbp, butfshrestores cytokinin levels to near normal by activating cytokinin biosynthesis genes. In addition, jasmonate levels in thefshsuppressor are significantly lower than inbp, which is likely due to elevated expression of JA inactivating genes. These observations suggest the involvement of the GSL pathway in generating one or more negative effectors of growth that influence inflorescence architecture and fecundity by altering the balance of hormonal regulators.