Cellular and Molecular Responses Unique to Major Injury Are Dispensable for Planarian Regeneration
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Author(s)
Tewari, Aneesha Gandhi
Stern, Sarah R.
Oderberg, Isaac Max
Reddien, Peter
Date Issued
November 2018
Journal
Cell Reports
Publisher
Elsevier
Citation
Tewari, Aneesha G. et al. “Cellular and Molecular Responses Unique to Major Injury Are Dispensable for Planarian Regeneration.” Cell Reports 25, 9 (November 2018): 2577–2590 © 2018 The Author(s)
Version
Final published version
Abstract
The fundamental requirements for regeneration are poorly understood. Planarians can robustly regenerate all tissues after injury, involving stem cells, positional information, and a set of cellular and molecular responses collectively called the “missing tissue” or “regenerative” response. follistatin, which encodes an extracellular Activin inhibitor, is required for the missing tissue response after head amputation and for subsequent regeneration. We found that follistatin is required for the missing tissue response regardless of the wound context, but causes regeneration failure only after head amputation. This head regeneration failure involves follistatin-mediated regulation of Wnt signaling at wounds and is not a consequence of a diminished missing tissue response. All tested contexts of regeneration, including head regeneration, could occur with a defective missing tissue response, but at a slower pace. Our findings suggest that major cellular and molecular programs induced specifically by large injuries function to accelerate regeneration but are dispensable for regeneration itself. In regenerative organisms, a large array of cellular responses are triggered at major injuries. However, which of these responses are fundamentally required for regeneration to occur remains unknown. Tewari et al. find that hallmark cellular and molecular responses induced uniquely at large injuries are dispensable for planarian regeneration. Keywords: regeneration; wound response; WnT signaling; TGF-β signaling; planarians; follistatin
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/j.celrep.2018.11.004
