par Fuks, François
Référence Bulletin et mémoires de l'Académie royale de médecine de Belgique, 163, 1-2, page (95-101; discussion 101-103)
Publication Publié, 2008
Article révisé par les pairs
Résumé : The nearly full sequence description of many eukaryotic genomes, including the human genome has shown that more complex eukaryotic model organisms (mammals) have a much bigger genome than less complex eukaryotes (e.g. flies), although the increased 'biocomplexity' is not reflected by an equivalent increase in the number of protein coding genes (e.g. > or = 30,000 in humans vs. approximately 15,000 in flies). These results strongly suggest that biocomplexity is only in part regulated by overall gene number, but largely depends on combinatorial control triggering a vast number of gene expression patterns. In addition, mechanisms other than DNA sequence information have been used during evolution to better index and regulate the complex developmental programmes and key regulatory processes, such as gene expression, chromosome segregation and cell division of eukaryotic genomes. "We are more than the sum of our genes", and have just entered a 'post-genomic' era that promises to define more clearly the molecular basis of our identity. DNA methylation and modified histones provide fundamental mechanisms for the function of most, if not all, chromatin-templated processes and link alterations in chromatin structure to gene expression patterns, dosage compensation, x inactivation, imprinting, developmental programming of cell lineages, the plasticity of stem cells and to genome stability. The implications of epigenetic research for human biology and disease, including cancer are far-reaching. While the field of epigenetic is exploding, the study of the mechanisms by which it plays fundamental roles within the cell are only beginning to emerge. Overall, deciphering these mechanisms represents the goal of our work.