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.