ABSTRACT

Using this assay, genetic screens were undertaken for mutations that perturbed the overall level of apoptosis in the embryo (White et a l , 1994). A collection of genomic deletions representing about half of the genome was screened for defects in apoptosis. In these screens, large numbers of embryos were collected from par­ ents heterozygous for a genomic deletion, and defects in apoptosis were analyzed in the 25% of the progeny homozygous for the deletion. Although most of these dele­ tions are large, deleting many functions that are required for normal embryonic development, the large supply of maternal gene products is generally sufficient to allow embryonic development to proceed long enough to assess apoptosis.