Newt orthologue of Growth arrest-specific 6 (NvGas6) is implicated in stress response during newt forelimb regeneration
Version of Record online: 27 JAN 2006
Copyright © 2006 Wiley-Liss, Inc.
Volume 235, Issue 3, pages 711–722, March 2006
How to Cite
Beug, S., Vascotto, S. G. and Tsilfidis, C. (2006), Newt orthologue of Growth arrest-specific 6 (NvGas6) is implicated in stress response during newt forelimb regeneration. Dev. Dyn., 235: 711–722. doi: 10.1002/dvdy.20690
- Issue online: 7 FEB 2006
- Version of Record online: 27 JAN 2006
- Manuscript Accepted: 16 DEC 2005
- Canadian Institutes of Health Research. Grant Number: 44055
- Natural Sciences and Engineering Research Council of Canada. Grant Number: 171259-00
- Notophthalmus viridescens;
- forelimb regeneration;
- stress response;
- cell survival
Red-spotted newts are capable of regenerating various structures and organs through the process of epimorphic regeneration. Receptor tyrosine kinases (RTKs) and their ligands are important for normal cellular development and physiology but most have not yet been characterised during regeneration. We have isolated a newt orthologue of Growth arrest-specific 6 (NvGas6), and examined its expression during forelimb regeneration and within a blastema cell line (B1H1). During limb regeneration, NvGas6 expression increases upon amputation, peaks during maximal blastema cell proliferation, and is subsequently downregulated during redifferentiation. Transcripts are localised to the wound epithelium and distal mesenchymal cells during dedifferentiation and proliferative phases, and scattered within redifferentiating tissues during later stages. In B1H1 cultures, NvGas6 is upregulated under reduced serum conditions and myogenesis. Treatment with mimosine and colchicine or exposure to heat shock or anoxia results in upregulation of NvGas6 expression. Taken together, our findings suggest that during regeneration, NvGas6 expression may be upregulated in response to cellular stress. Developmental Dynamics 235:711–722, 2006. © 2006 Wiley-Liss, Inc.