The mitochondrial TOM complex modulates bax-induced apoptosis in Drosophila.
Bax is a pro-apoptotic member of the Bcl-2 family proteins involved in the release of apoptogenic factors from mitochondria to the cytosol. Recently, it has been shown both in mammals and yeast that Bax insertion in the mitochondrial outer membrane involves at least two distinct mechanisms, one of which uses the TOM complex. Here, we show that in Drosophila, heterozygous loss of function mutations of Tom22 or Tom70, two receptors of the TOM complex, attenuates bax-induced phenotypes in vivo. These results argue that the TOM complex may be used as a mitochondrial Bax receptor in Drosophila.
Colin
J
J
Laboratoire de Génétique et Biologie Cellulaire, Université de Versaillers Saint-Quentin-en-Yvelines, CNRS UMR 8159, 45 avenue des Etats-Unis, F-78035 Versailles cedex, France.
Garibal
J
J
Mignotte
B
B
Guénal
I
I
D000818:Animals; D017209:Apoptosis; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000166:cytology / Q000201:enzymology / Q000502:physiology*; D008928:Mitochondria / Q000201:enzymology*; D000090622:Mitochondrial Precursor Protein Import Complex Proteins; D009154:Mutation; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
D002352:Carrier Proteins; D000090622:Mitochondrial Precursor Protein Import Complex Proteins; D051028:bcl-2-Associated X Protein