The rapid engulfment of apoptotic cells is a specialized immune response used by organisms to remove the "nonself", apoptotic cells, and it is an inevitable second part of apoptosis. In vivo, the engulfment process is a swift and efficient process and usually takes place at a very early stage of apoptosis, it prevents the release of potentially harmful contents from dying cells to injure the surrounding tissue. In C. elegans , seven genes,
ced-1 , -2 , -5 , -6 , -7 , -10 and -12 have been identified to affect the engulfment process. The genetic and the phenotypic studies have put
ced-1 , -6 , and -7 into one group, and
ced-2 , -5 , and -10 into another. Genetic studies also demonstrated that
ced-6 might act downstream of both
ced-1 and
ced-7 . We have previously cloned
ced-6 . This gene encodes a novel protein that contains a phosphotyrosine binding (PTB) domain at its N-termini and a potential SH3 binding sites at its C-terminal half. By genetic mosaic analysis
ced-6 has been demonstrated to act within engulfing cells. CED-6 might be an adaptor molecule that acts in a tyrosine kinase pathway that is specifically required for engulfing cells to remove apoptotic cells. To understand whether the CED-6 engulfment pathway is conserved in species, we have isolated potential
ced-6 homologues from other species including human. These CED-6 homologues are very similar to C. elegans CED-6 structurally. Overexpression of hCED-6 in C. elegans can rescue the engulfment defect in the
ced-6 mutant animals, suggesting that hCED-6 might be a functional homologue of C. elegans CED-6. Thus, CED-6, and the CED-6 signal transduction pathway is likely to be conserved from C. elegans to man.