MITOCHONDRIAL CONTROL OF APOPTOSIS - DID PROGRAMMED CELL-DEATH APPEARAFTER THE ENDOSYMBIOTIC EVENT GIVING RISE TO MITOCHONDRIA

Most animal cells can undergo a process of programmed cell,death calle d apoptosis. Cellular proteins involved in this-self-destruction proce ss have changed relatively little since the divergence of nematodes an d vertebrates. It appears now that mitochondria occupy a strategic pla ce in the control of apoptosis. In mammals, as well as in nematodes, p rotein of the Bcl-2/Bcl-X/Ced-9 family inhibit apoptosis at least at t wo levels: regulation of membrane permeability to ions or pro-apoptoti c molecules, and anchorage to the mitochondria of proteins involved in the transduction of apoptotic signals. It is now accepted that mitoch ondria are endosymbionts, originating in aerobic bacteria which were i ntegrated by the ancestor of eukaryotic cells. A part of the apoptotic machinery would exist in unicellular eukaryotes and some components c ontrolling apoptosis might he 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 t he host cell precursor of eukaryotes, provided the basis for the actua l mechanism controlling cell survival. Metazoans would have exploited this possibility by connecting the mitochondrial effectors of cellular death to the pathways of signal transduction.