Unusually for mammals, rodent incisors grow continuously, fuelled by stem cells in their mesenchymal and epithelial compartments. Constant abrasion of the incisor's lingual side (the side facing the tongue), which unlike the opposite side has no hard enamel covering, maintains its length and shape. But why is enamel produced asymmetrically? On , Gail Martin and co-workers report that sprouty (Spry) genes, which encode FGF signalling antagonists, ensure this asymmetrical enamel deposition and prevent the growth of tusk-like incisors. The researchers show that enamel-producing ameloblasts develop from stem cells on both sides of the incisors of Spry4-/- mouse embryos and that an ectopic epithelial-mesenchymal FGF signalling loop on the lingual side of the incisors causes this phenotype. Interestingly, ectopic ameloblast formation is maintained after birth only if the dosage of Spry1 or Spry2is also reduced. Thus, the researchers suggest, the generation of differentiated progeny (such as ameloblasts) from stem cell populations can be differentially regulated in embryos and adults.
