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The interaction between signaling pathways is a central question in the study of organogenesis. Using the developing murine tongue as a model, we uncovered unknown relationships between Sonic hedgehog (SHH) and retinoic acid (RA) signaling. Genetic loss of SHH signaling leads to enhanced RA activity subsequent to loss of SHH-dependent expression of Cyp26a1 and Cyp26c1. This causes a cell identity switch, prompting the epithelium of the tongue to form heterotopic minor salivary glands and to overproduce oversized taste buds. At developmental stages during which Wnt10b expression normally ceases and Shh becomes confined to taste bud cells, loss of SHH inputs causes the lingual epithelium to undergo an ectopic and anachronic expression of Shh and Wnt10b in the basal layer, specifying de novo taste placode induction. Surprisingly, in the absence of SHH signaling, lingual epithelial cells adopted a Merkel cell fate, but this was not caused by enhanced RA signaling. We show that RA promotes, whereas SHH, acting strictly within the lingual epithelium, inhibits taste placode and lingual gland formation by thwarting RA activity. These findings reveal key functions for SHH and RA in cell fate specification in the lingual epithelium and aid in deciphering the molecular mechanisms that assign cell identity., Author summary Knowledge of the biological mechanisms controlling cell fate specification is of paramount importance for cell-based therapies. Sonic hedgehog (SHH) and retinoic acid (RA) pathways play key roles in development and disease. The role of SHH during in vivo tongue development is a subject of great interest, and whether RA signaling has any function in the developing tongue is unknown. The tongue is covered by a mucosa made of lingual epithelium and lingual mesenchyme. Various structures, including mechanosensory filiform papillae, gustatory papillae harboring taste buds, and minor salivary glands, arise from the epithelium, but how these entities are specified remains unclear. Here we show that in the mesenchyme SHH signaling drives growth and morphogenesis, whereas in the epithelium, SHH controls patterning and cell fate specification. We demonstrate that SHH inhibits taste placode and lingual gland formation by antagonizing RA inputs. We also show that loss of SHH signaling elicits Merkel cell formation in the lingual epithelium, a tissue normally bereft of Merkel cells. This is at odds with the hairy epidermis where Merkel cell specification has been shown to be SHH-dependent. Our study establishes SHH and RA as key players in the control of cell identity within the lingual epithelium.