Fig. 1. Cell fate transformations in the T.pp lineage in sem-4 animals. Lineage diagrams of the wild-type T.pp, AB.p(l/r)apappp and QL lineages (top) and the variable T.pp lineage in sem-4 animals (bottom). Cell deaths are indicated with an `X'. Cells in parentheses exhibit abnormal morphologies or migration patterns. Cells that expressed the mec-3::gfp reporter are indicated with a `mec-3'. The proportion of sem-4 animals in which T.pp adopted each fate (only one side was examined per animal) is shown beneath the lineage diagrams. Of the 18 animals in which T.ppa did not divide, T.ppa died in nine and lived in nine. In four out of 23 animals, T.ppa divided and gave rise to an anterior daughter that died and a posterior daughter that migrated ventrally and then began to express mec-3::gfp. In a fifth animal, T.ppa divided and the posterior daughter migrated to the ventral side but the worm died before the lineage was completed. While examining these lineages, we found that loss of sem-4 function not only induced apoptosis in a cell that should normally differentiate (T.ppa), but also sometimes induced deaths that appeared to be necrotic, both in T.ppa and in a cell that normally undergoes apoptosis (T.pppp). These necrotic deaths were characterized by the formation of large vacuoles, similar to those induced by gain-of-function mutations in degenerin genes (Chalfie and Wolinsky, 1990; Hall et al., 1997). T.pppp died as a vacuolated cell in one of the five lineages in which T.ppa divided and in two of the nine lineages in which T.ppa lived; in all nine lineages in which T.ppa died, T.pppp underwent apoptosis. T.ppa itself died as a vacuolated cell in three out of nine lineages. The egl-5 gene was ectopically expressed both in cells undergoing apoptosis and in cells undergoing necrosis in sem-4 animals.

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