A wound-induced Wnt expression program controls planarian regeneration polarity

  1. Christian P. Petersena and
  2. Peter W. Reddiena,b,1
  1. aWhitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142; and
  2. bDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02142
  1. Edited by Terry L. Orr-Weaver, Massachusetts Institute of Technology, Cambridge, MA, and approved August 10, 2009 (received for review June 19, 2009)

Abstract

Regeneration requires specification of the identity of new tissues to be made. Whether this process relies only on intrinsic regulative properties of regenerating tissues or whether wound signaling provides input into tissue repatterning is not known. The head-versus-tail regeneration polarity decision in planarians, which requires Wnt signaling, provides a paradigm to study the process of tissue identity specification during regeneration. The Smed-wntP-1 gene is required for regeneration polarity and is expressed at the posterior pole of intact animals. Surprisingly, wntP-1 was expressed at both anterior- and posterior-facing wounds rapidly after wounding. wntP-1 expression was induced by all types of wounds examined, regardless of whether wounding prompted tail regeneration. Regeneration polarity was found to require new expression of wntP-1. Inhibition of the wntP-2 gene enhanced the polarity phenotype due to wntP-1 inhibition, with new expression of wntP-2 in regeneration occurring subsequent to expression of wntP-1 and localized only to posterior-facing wounds. New expression of wntP-2 required wound-induced wntP-1. Finally, wntP-1 and wntP-2 expression changes occurred even in the absence of neoblast stem cells, which are required for regeneration, suggesting that the role of these genes in polarity is independent of and instructive for tail formation. These data indicate that wound-induced input is involved in resetting the normal polarized features of the body axis during regeneration.

Footnotes

  • 1To whom correspondence should be addressed. E-mail: reddien{at}wi.mit.edu
  • Author contributions: C.P.P. and P.W.R. designed research; C.P.P. performed research; C.P.P. and P.W.R. analyzed data; and C.P.P. and P.W.R. wrote the paper.

  • The authors declare no conflict of interest.

  • This article is a PNAS Direct Submission.

  • This article contains supporting information online at www.pnas.org/cgi/content/full/0906823106/DCSupplemental.

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