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First published online 17 October 2007
doi: 10.1242/dev.007138

Development 134, 4043-4051 (2007)
Published by The Company of Biologists 2007
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BMP signaling regulates the dorsal planarian midline and is needed for asymmetric regeneration

Peter W. Reddien1, Adam L. Bermange2,*, Adrienne M. Kicza1 and Alejandro Sánchez Alvarado2,{dagger}

1 MIT Biology, Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02138, USA.
2 Howard Hughes Medical Institute, Department of Neurobiology and Anatomy, University of Utah School of Medicine, 401 MREB, 20N 1900E, Salt Lake City, UT 84132, USA.

{dagger} Author for correspondence (e-mail: sanchez{at}neuro.utah.edu)

Accepted 25 August 2007

Planarians can be cut into irregularly shaped fragments capable of regenerating new and complete organisms. Such regenerative capacities involve a robust ability to restore bilateral symmetry. We have identified three genes needed for bilaterally asymmetric fragments to regenerate missing body parts. These genes are candidate components of a signaling pathway that controls the dorsal-ventral patterning of many animal embryos: a BMP1/Tolloid-like gene (smedolloid-1), a SMAD4-like gene (smedsmad4-1), and a BMP2/4/DPP-like gene (smedbmp4-1). BMP signaling was involved in the formation of new tissues at the midline of regeneration, the dorsal-ventral patterning of new tissues, and the maintenance of the dorsal-ventral pattern of existing adult tissue in homeostasis. smedbmp4-1 was normally expressed at the dorsal midline. Asymmetric fragments lacking a midline displayed new smedbmp4-1 expression prior to formation of a regenerative outgrowth (blastema). Asymmetric fragments containing the midline displayed expanded smedbmp4-1 expression towards the wound. We suggest injured animals that lack left-right symmetry reset their midline through modulation of BMP activity as an early and necessary event in regeneration.

Key words: Asymmetry, BMP, Planaria, Regeneration, Adult homeostasis


Related articles in Development:

From fragments to whole: BMP signals regeneration

Development 2007 134: e2205. [Full Text]  



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