During Arabidopsis embryonic development, the cotyledons form from precursors that do not derive from the shoot apical meristem, from which the other leaves form. The role of auxin and the genes involved in this process are unknown. Now, on p. 4063, Treml et al. report a novel Arabidopsis mutant, laterne, in which,unusually, cotyledons are specifically and precisely lost. This mutant carries mutations in PINOID, which helps localise the PIN1 auxin transport facilitator to the apical membrane of meristem epidermal cells, and in ENHANCER OF PINOID (ENP), a novel gene of unknown function. In laterne plants, the authors report, the normal apical localisation of PIN1 is reversed to basal, which is likely to cause apical cells in the embryo to repulse auxin coming from basal cells. Consequently, auxin, which is essential for organ formation, fails to accumulate in the mutant cotyledon primordia. Future studies should elucidate the exact role of ENP in auxin transport.