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Regeneration is widespread, but mechanisms that activate regeneration remain mysterious. Planarians are capable of whole-body regeneration and mount distinct molecular responses to wounds that result in tissue absence and those that do not. A major question is how these distinct responses are activated. We describe a follistatin homolog ( Smed-follistatin ) required for planarian regeneration.  Smed-follistatin  inhibition blocks responses to tissue absence but does not prevent normal tissue turnover. Two activin homologs ( Smed-activin-1  and  Smed-activin-2 ) are required for the  Smed-follistatin  phenotype. Finally,  Smed-follistatin  is wound-induced and expressed at higher levels following injuries that cause tissue absence. These data suggest that Smed-follistatin inhibits Smed-Activin proteins to trigger regeneration specifically following injuries involving tissue absence and identify a mechanism critical for regeneration initiation, a process important across the animal kingdom.

Tissue absence initiates regeneration through Follistatin-mediated inhibition of Activin signaling