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First published online March 1, 2007
doi: 10.1242/10.1242/dev.002220


1 Department of Zoology, Graduate School of Science, Kyoto University, Sakyo-ku,
Kyoto 606-8502, Japan.
2 Department of Biology, Graduate School of Science, Osaka University, 1-1
Machikaneya-cho, Toyonaka, Osaka 560-0043, Japan.
3 Department of Marine Biotechnology, Faculty of Life Science and Biotechnology,
Fukuyama University, Fukuyama 729-0292, Japan.
4 UMR 7009, Centre National de la Recherche Scientifique/Université
Pierre et Marie Curie, Biologie du Développement, Observatoire
Océanologique de Villefranche-sur-Mer, quai de la Darse-06234
Villefranche-sur-Mer Cedex, France.
Authors for correspondence (e-mail:
jean-philippe.chambon{at}obs-vlfr.fr;
satoh{at}ascidian.zool.kyoto-u.ac.jp)
Accepted 11 January 2007
In ascidian tadpoles, metamorphosis is triggered by a polarized wave of apoptosis, via mechanisms that are largely unknown. We demonstrate that the MAP kinases ERK and JNK are both required for the wave of apoptosis and metamorphosis. By employing a gene-profiling-based approach, we identified the network of genes controlled by either ERK or JNK activity that stimulate the onset of apoptosis. This approach identified a gene network involved in hormonal signalling, in innate immunity, in cell-cell communication and in the extracellular matrix. Through gene silencing, we show that Ci-sushi, a cell-cell communication protein controlled by JNK activity, is required for the wave of apoptosis that precedes tail regression. These observations lead us to propose a model of metamorphosis whereby JNK activity in the CNS induces apoptosis in several adjacent tissues that compose the tail by inducing the expression of genes such as Ci-sushi.
Key words: Ascidian tadpoles, Apoptosis, Ci-sushi, Metamorphosis, MAPK
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