Redox-modulated ERK dynamics support wound-dependent tissue formation during early planarian regeneration.

19 , 20 Wnt1 expression is rapidly increased at the wound site, activating β-catenin predominantly in the posterior region, with a decreasing trend along the A-P axis. 12 , 21 While Wnt/β-catenin signaling specifies posterior identity, anterior regeneration is promoted by a distinct set of factors, including the Wnt inhibitor notum, the activin antagonist follistatin, and the transcription factors runt-1 and early growth response protein 4 (eg

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