CONTROLE MITOCHONDRIAL DE L'APOPTOSE: LA MORT CELLULAIRE PROGRAMMEE EST-ELLE APPARUE A LA SUITE DE L'EVENEMENT ENDOSYMBIOTIQUE A L'ORIGINE DES MITOCHONDRIES?

Most animal cells can undergo a process of programmed cell death called apoptosis. Cellular proteins involved in this self-destruction process have changed relatively little since the divergence of nematodes and vertebrates. It appears now that mitochondria occupy a strategic place in the control of apoptosis. In mammals, as well as in nematodes, proteins of the Bcl-2/Bcl-X/Ced-9 family inhibit apoptosis at least at two levels: regulation of membrane permeability to ions or pro-apoptotic molecules, and anchorage to the mitochondria of proteins involved in the transduction of apoptotic signals. It is now accepted that mitochondria are endosymbionts, originating in aerobic bacteria which were integrated by the ancestor of eukaryotic cells. A part of the apoptotic machinery could exist in unicellular eukaryotes and some components controlling apoptosis might be present in prokaryotes. It is therefore possible that the mechanism originally involved in the maintenance of the symbiosis between the bacterial ancestor of the mitochondria and the host cell precursor of eukaryotes, provided the basis for the actual mechanism controlling cell survival. Metazoans would have exploited this possibility by connecting the mitochondrial effecters of cellular death to the pathways of signal transduction.