Tissue absence initiates regeneration through Follistatin-mediated inhibition of Activin signaling
Author(s)Gavino, Michael A.; Wenemoser, Danielle; Wang, Irving E.; Reddien, Peter
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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.
DepartmentMassachusetts Institute of Technology. Department of Biology; Whitehead Institute for Biomedical Research
eLife Sciences Publications, Ltd.
Gavino, M. A., D. Wenemoser, I. E. Wang, and P. W. Reddien. “Tissue Absence Initiates Regeneration through Follistatin-Mediated Inhibition of Activin Signaling.” eLife 2, no. 0 (September 10, 2013): e00247–e00247.
Final published version