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Epithelial-mesenchymal interactions are crucial for the development of numerous animal structures. Thus, unraveling how molecular tools are recruited in different lineages to control interplays between these tissues is key to understanding morphogenetic evolution. Here, we study  Esrp  genes, which regulate extensive splicing programs and are essential for mammalian organogenesis. We find that  Esrp  homologs have been independently recruited for the development of multiple structures across deuterostomes. Although  Esrp  is involved in a wide variety of ontogenetic processes, our results suggest ancient roles in non-neural ectoderm and regulating specific mesenchymal-to-epithelial transitions in deuterostome ancestors. However, consistent with the extensive rewiring of  Esrp -dependent splicing programs between phyla, most developmental defects observed in vertebrate mutants are related to other types of morphogenetic processes. This is likely connected to the origin of an event in  Fgfr , which was recruited as an  Esrp  target in stem chordates and subsequently co-opted into the development of many novel traits in vertebrates.

Evolutionary recruitment of flexible Esrp-dependent splicing programs into diverse embryonic morphogenetic processes