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In mammals, the embryo develops through a progressive posterior elongation process such that the first structures formed are the anterior ones while more posterior ones are added successively. This developmental strategy implies that growth and patterning of the embryo must be tightly coordinated. As far as patterning is concerned, it relies, at least in part, upon the function of the Hox family of transcription factors. In mammals, there are 39 Hox genes grouped in four complexes (HoxA, HoxB, HoxC and HoxD). The functional distribution of these genes along the anterior-posterior (A-P) axis of the embryo, which underlies the ultimate body architecture, is tightly linked to their genomic organization. Indeed, the linear order of the genes within a complex is collinear to their sequence of transcriptional activation, both in time and space.

Recent experiments have identified direct interactions between Hox proteins and regulators of the cell cycle and apoptosis. The data obtained suggest that Hox proteins have the ability to control cell proliferation and apoptosis but little is known about this functional property of the Hox gene family. We are interested in understanding the relationships between Hox genes and the regulation of cell proliferation and apoptosis during embryo morphogenesis. We have previously shown that limbs deprived of Hox functions have severe growth defects and we are currently investigating the molecular pathways that link Hox genes to growth processes during embryonic development. Our goal is to unravel the mechanisms whereby growth and patterning are coordinated during embryogenesis and gain further insights into the processes whereby the body architecture is set up.

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