In
cdl-1 (cell death lethal) mutants, several embryonic defects are observed: 1) excess cell corpses in late embryogenesis, 2) variable defects in elongation, 3) failure in attachment of the pharynx to the buccal cavity. There are three existing
cdl-1 alleles,
e2510,
e2501 and
w37. They differ mainly in their severity of the elongation defect; the ratios of the homozygous embryos to reach to pretzels at 20C! are: 6% in
e2510, 50% in
e2501 and 60% in
w37. Regardless of the extent of the elongation, the pharynx defect is 100% penetrant in all alleles. The number of excess cell corpses seen in the terminal embryos is smaller in
w37 than other alleles. The lethality of
cdl-1 is not directly caused by the production of excess corpses per se, because neither
ced-3,
ced-4 nor
ced-9(gf) mutations rescue the lethality and elongation defect of
cdl-1 mutations, although they suppress the production of corpses in the
cdl-1 mutant embryos. The excess cell corpses in
cdl-1 might be the accumulated corpses due to the defect in the engulfment process. In the double mutants of
cdl-1 with either
ced-1 or
ced-5 (mutants of the genes that belong to distinct engulfment pathways), the number of cell corpses dramatically increased compared to that in each single mutant, suggesting that
cdl-1 is not a member of the known engulfment pathways. Thus,
cdl-1 may define a new group of engulfment genes, or may be involved in the common process in the two engulfment pathways. In addition, we cannot exclude the possibility that
cdl-1 is involved in the death/life decision of the cells. To identify the gene product of
cdl-1, we initiated cloning of the gene. It was mapped to the right of
dpy-10 on LG II. mnDf89, mnDf90 and mnDf83 failed to, but mnDf87 did complement the lethality of
cdl-1 mutants, thus narrowing the genomic region to <1 map unit. Recently we have identified a cosmid that rescues the lethality of
cdl-1 by transformation rescue. We are currently trying to narrow down the rescuing activity further.