Mesenchymal sculpting is a major driver of organogenesis. (A) Mesenchymal sculpting in gut and lung. (A1) In the developing gut, tissue shape emerges through coordinated interactions between the muscle and epithelium. In birds, muscle compression, combined with the elasticity of the epithelium, is essential for vilification (the formation of villi). In mice, active mesenchymal migration and dewetting behavior drive the formation of droplet-like mesenchymal aggregates. In Drosophila, muscle contractions steer gut looping by inducing epithelial shape changes in the underlying endoderm. (A2) In the lung, airway smooth muscle cells undergo intercalation to sculpt the branching airways. In the distal lung, the undifferentiated mesenchyme surrounding the developing saccules must remain fluid-like, providing the compressibility required for proper sacculation. (B) Mesenchymal sculpting of the Drosophila testis. (B1) Unlike other internal organs, the Drosophila testis is initially free of muscles. TNMs migrate collectively from the genital disk onto the testis surface beneath a layer of motile and squamous pigment cells (not depicted for simplicity). (B2 and B3) As the testis grows and loops into a spiral, TNMs undergo mesenchymal intercalation, reshaping the tissue. (B4) During migration, TNMs extend protrusions in all directions, but protrusions at cell–cell contacts exhibit reduced matrix adhesion, promoting expansion toward free edges. Simultaneously, PlexA maintains some matrix adhesion at contacts, enabling cells to spread dynamically during migration—an essential feature for sheet integrity. (B5) Disruption of migration or sheet integrity during migration impairs testis morphogenesis: the muscle layer fails to sculpt the organ, resulting in characteristic defects. In the complete absence of TNMs, the testis fails to coil and instead remains an ellipsoid.