Edgar (Ned) Buttner
Research Associate
nedbuttner[at]mcb[dot]harvard[dot]edu
Research Area:
Germ Line
Germline
We have analyzed the germline proliferation defects caused by depletion of the C. elegans lissencephaly disease gene homolog lis-1 and have shown that loss of lis-1 activates the spindle checkpoint resulting in mitotic arrest, followed by ced-3-dependent programmed cell death (apoptosis). These results place the spindle checkpoint pathway upstream of the programmed cell death pathway and suggest that apoptosis may contribute to the cell-sparse pathology of lissencephaly.