Tissue absence initiates regeneration through Follistatin-mediated inhibition of Activin signaling
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Reddien_Tissue absence.pdf
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Author(s)
Gavino, Michael A.
Wenemoser, Danielle
Wang, Irving E.
Reddien, Peter
Date Issued
September 2013
Journal
eLife
Publisher
eLife Sciences Publications, Ltd.
Citation
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.
Version
Final published version
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Whitehead Institute for Biomedical Research
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DOI of Published Version
https://doi.org/10.7554/eLife.00247
