Spry can block TGFβ-mediated signaling in lens cells. Representative sections of neonatal WT mouse lenses (A, A’, B, B’, C, C’), or transgenic mouse lenses overexpressing TGFβ1 (D, D’, E, E’, F, F’; TGFβ) or both TGFβ1 and Spry1 (G, G’, H, H’, I, I’; TGFβ/Spry1), immunolabelled for either pSmad2 (A’, D’, G’), Snai1 (B’, E’, H’) or Snai2 (C’, F’, I’), with cell nuclei counterstained with Hoechst dye (A–I). Compared to WT lens epithelia (le) that do not display nuclear reactivity for pSmad2 (A’), Snai1 (B’) or Snai2 (C’), lens cells in transgenic mice stimulated by elevated levels of TGFβ demonstrate a clear nuclear label for all three of these TGFβ-mediated signaling molecules (D’, E’, F’; arrows). In lens epithelial cells (le) of transgenic mice overexpressing TGFβ and Spry, there is no nuclear labeling for pSmad2 (G’), Snai1 (H’) or Snai2 (I’), similar to that seen in WT mice. Scale bar, 20 µm.