TBid mediated activation of the mitochondrial death pathway leads to genetic ablation of the lens in Xenopus laevis
✍ Scribed by D. Du Pasquier; A. Chesneau; Q. Ymlahi-Ouazzani; R. Boistel; N. Pollet; C. Ballagny; L.M. Sachs; B. Demeneix; A. Mazabraud
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 741 KB
- Volume
- 45
- Category
- Article
- ISSN
- 1526-954X
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✦ Synopsis
Abstract
Xenopus is a well proven model for a wide variety of developmental studies, including cell lineage. Cell lineage in Xenopus has largely been addressed by injection of tracer molecules or by micro‐dissection elimination of blastomeres. Here we describe a genetic method for cell ablation based on the use of tBid, a direct activator of the mitochondrial apoptotic pathway. In mammalian cells, cross‐talk between the main apoptotic pathways (the mitochondrial and the death domain protein pathways) involve the pro‐death protein BID, the active form of which, tBID, results from protease truncation and translocation to mitochondria. In transgenic Xenopus, restricting tBID expression to the lens‐forming cells enables the specific ablation of the lens without affecting the development of other eye structures. Thus, overexpression of tBid can be used in vivo as a tool to eliminate a defined cell population by apoptosis in a developing organism and to evaluate the degree of autonomy or the inductive effects of a specific tissue during embryonic development. genesis 45:1–10, 2007. © 2006 Wiley‐Liss, Inc.