Loss-of-function mutations in the gene ced-8 lead to the late appearance of
cell corpses during embryonic development in C. elegans. ced-8 functions d
ownstream of or in parallel to the regulatory cell death gene ced-9 and may
function as a cell death effector downstream of the caspase encoded by the
programmed cell death killer gene ced-3. In ced-8 mutants, embryonic progr
ammed cell death probably initiates normally but proceeds slowly, ced-8 enc
odes a transmembrane protein that appears to be localized to the plasma mem
brane. The CED-8 protein is similar to human XK, a putative membrane transp
ort protein implicated in McLeod Syndrome, a form of hereditary neuroacanth
ocytosis.