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.

On Death and Dying in C. elegans

H.M. Ellis, B. Horvitz

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 
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.