Generic wound signals initiate regeneration in missing-tissue contexts

Suthira Owlarn, Felix Klenner, David Schmidt, Franziska Rabert, Antonio Tomasso, Hanna Reuter, Medhanie A. Mulaw, Sören Moritz, Luca Gentile, Gilbert Weidinger () and Kerstin Bartscherer ()
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Suthira Owlarn: Max Planck Institute for Molecular Biomedicine
Felix Klenner: Ulm University
David Schmidt: Max Planck Institute for Molecular Biomedicine
Franziska Rabert: Max Planck Institute for Molecular Biomedicine
Antonio Tomasso: Max Planck Institute for Molecular Biomedicine
Hanna Reuter: Max Planck Institute for Molecular Biomedicine
Medhanie A. Mulaw: Ulm University
Sören Moritz: Max Planck Institute for Molecular Biomedicine
Luca Gentile: Max Planck Institute for Molecular Biomedicine
Gilbert Weidinger: Ulm University
Kerstin Bartscherer: Max Planck Institute for Molecular Biomedicine

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Despite the identification of numerous regulators of regeneration in different animal models, a fundamental question remains: why do some wounds trigger the full regeneration of lost body parts, whereas others resolve by mere healing? By selectively inhibiting regeneration initiation, but not the formation of a wound epidermis, here we create headless planarians and finless zebrafish. Strikingly, in both missing-tissue contexts, injuries that normally do not trigger regeneration activate complete restoration of heads and fin rays. Our results demonstrate that generic wound signals have regeneration-inducing power. However, they are interpreted as regeneration triggers only in a permissive tissue context: when body parts are missing, or when tissue-resident polarity signals, such as Wnt activity in planarians, are modified. Hence, the ability to decode generic wound-induced signals as regeneration-initiating cues may be the crucial difference that distinguishes animals that regenerate from those that cannot.

Date: 2017
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DOI: 10.1038/s41467-017-02338-x

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