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Chordate metamorphosis is a postembryonic larva-to-juvenile transition triggered by thyroid hormones and their specific receptors (TR). This crucial developmental event shows a wide morphological diversity among different chordate lineages and is characterized by ecological, morphological, metabolic and behavioral changes that can be drastic. One of the most studied models is the amphibian Xenopus, whose tadpole metamorphosis includes apoptosis-induced tail regression dependent on the thyroid hormone pathway. In an evolutionary context, we used the ascidian model, the extant closest group to vertebrates, in which the swimming larva transforms to a sessile filter-feeding juvenile during metamorphosis, to study the role of thyroid hormones in this transformation. The ascidian metamorphosis is also characterized by an apoptosis-driven tail regression as in Xenopus. However, whether this apoptosis-driven process is dependent on the thyroid hormone has not yet been elucidated.In this study, we interfered with thyroid hormone signaling during tail regression of the ascidianCiona robustato investigate whether (i) thyroid hormone is involved in the regulation of developmental apoptosis, and (ii) apoptosis leading to tail regression involves its classical molecular pathways. We described specific gene expression landmarks as well as apoptosis dynamics during larva metamorphosis under thyroid hormone exposure and thyroid hormone inhibition treatments. We provide evidence thatCiona robustametamorphosis involves thyroid hormone-dependent apoptosis, similar to other studied chordates. However, the mode of action of thyroid hormone shows great variation compared to the classically described scheme in chordates, both in thyroid hormone/TR interactions and in the apoptotic pathway.

International audience; Previous studies have addressed why and how mono‐stratified epithelia adopt a polygonal topology. One major additional, and yet unanswered question is how the frequency of different cell shapes is achieved and whether the same distribution applies between non-prolifer-ative and proliferative epithelia. We compared different proliferative and non-proliferative epithelia from a range of organisms as well as Drosophila melanogaster mutants, deficient for apoptosis or hyperproliferative. We show that the distribution of cell shapes in non‐prolif-erative epithelia (follicular cells of five species of tunicates) is distinctly, and more stringently organized than proliferative ones (cultured epithelial cells and Drosophila melanogaster imaginal discs). The discrepancy is not supported by geometrical constraints (spherical versus flat monolayers), number of cells, or apoptosis events. We have developed a theoretical model of epithelial morphogenesis, based on the physics of divided media, that takes into account biological parameters such as cell‐cell contact adhesions and tensions, cell and tissue growth, and which reproduces the effects of proliferation by increasing the topological heterogeneity observed experimentally. We therefore present a model for the morphogene-sis of epithelia where, in a proliferative context, an extended distribution of cell shapes (range of 4 to 10 neighbors per cell) contrasts with the narrower range of 5-7 neighbors per cell that characterizes non proliferative epithelia.