Worm Breeder's Gazette 7(1): 67
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Programmed cell death is a prominent feature of both the embryonic and postembryonic cell lineages of C. elegans. We have recently isolated two new classes of mutations affecting cell death. In one class cells that normally die instead survive, and in the other class cells that normally survive instead die. These mutants were isolated by mutagenizing ced-1(e1735) I, a mutation that prolongs the highly refractile stage of cell death (kindly given to us by Ed Hedgecock; see Newsletter Vol. 5, No. 2), and screening F2 progeny for extra or missing deaths. Two mutations in the gene ced(n717, n718) IV define the first class of mutations mentioned above. The late embryonic and early postembryonic deaths, which can normally be seen in L1 and L2 larvae of ced-1, are not seen in ced-1; n717 and ced-1; n718. Instead, extra neuronal-like nuclei are generated in several lineages that normally include deaths: the Q1 and V5.pa lineages of ced-1; n717 are identical to those of N2 except that cells that normally die form small compact nuclei. Thus, n717 and n718 appear to suppress the phenotype of ced-1 by acting prior to ced-1.Further characterization of the fate of the extra cells in ced(n717) may aid us in understanding the role of cell death in C. elegans development. For instance, it is conceivable that cell death functions to eliminate blast cells. However, no extra divisions occur in the Q1, V5.pa or Pn.a lineages of these mutants. Although embryonic lineages have not been determined in ced(n717), there is no evidence at hatching of grossly abnormal cell proliferation during embryonic growth. It seems more likely that programmed cell death eliminates cells that would otherwise differentiate. FIF staining of ced-1; n717 reveals an extra dopamine- containing cell in the postdeirid; the extra dopamine cell is probably V5.paapp, the cell that normally dies. We have also examined the fate of the normally male-specific cephalic companion cells in ced-1; n717 hermaphrodites. The cephalic companions have been suggested to play a role in male attraction to hermaphrodites. John Sulston has found that in N2 hermaphrodites the cells lineally equivalent to the cephalic companions die during embryonic development. In ced-1; n717 L4 hermaphrodites, the cephalic companions can be identified by their characteristically large nucleoli. However, adult ced-1; n717 hermaphrodites do not track toward other hermaphrodites. Based on these observations, it seems likely that cells that fail to die in ced(n717) generally differentiate. Given the large number of programmed cell deaths in the embryonic and postembryonic lineages, it is interesting that neither n717 nor n718 has any noticeable defects in behavior or morphology visible at the level of the dissecting microscope. The recessive mutation n709(III) results in extra cell deaths in the ventral cord. In N2, Pn.aap dies in the lineages of P1, P2, and P9- P12, while P3.aap-P8.aap survive and differentiate into VC neurons. In n709, Pn.aap deaths occur in the P3-P8 lineages as well as in the P1, P2, and P9-P12 lineages. By Nomarski criteria, the extra deaths appear indistinguishable from those that normally occur in the ventral cord. Counting ventral cord neuronal nuclei in DAPI-stained animals shows that the number of extra deaths in n709 ranges from one to six. Lineage studies have confirmed the variable expressivity of n709. Extra deaths have not been observed in any other postembryonic lineages of n709.