Worm Breeder's Gazette 8(3): 50

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.

Mutations Causing Neuronal Degeneration

M. Chalfie

The mutation e1611 is a dominant allele of mec-4.  The touch cells 
in animals carrying this mutation degenerate (Chalfie and Sulston, 
Develop.  Biol.  82: 358-370, 1981).  In a recent screen for touch-
insensitive mutants, 28 additional mec-4 mutations were isolated.  Of 
these 26 are recessive, and although the animals are touch insensitive,
the touch cells do not die.  Two of the new alleles are dominants, 
and animals carrying either have touch cells that degenerate.  The 
effects of the mutations seem quite specific for the touch cells since 
no other cells degenerate in these mutants.
In the same screen a rather unusual touch mutant was identified.  
This animal was touch-insensitive only on the tail, and did not 
respond to the touch of fine hair or to prodding with a platinum wire (
mec mutants respond to the wire, but not the hair).  This mutation, 
deg-1(u38) X is dominant.  The mutation has not been separated for mec-
7 (p<0.06%).  The touch cells are normal, but the PVC interneurons 
degenerate (these interneurons appear to be the most important 
postsynaptic targets of the touch cells in the tail; Chalfie et al., J.
Neurosci., in press).  The degeneration, which has the same 
vacuolated appearance of the touch cell deaths in the dominant mec-4 
mutants, occurs 12-24 hrs after hatching at 250.  The mutation is 
temperature sensitive; the temperature-critical period corresponds to 
the time of the PVC cell deaths.  The PVC interneurons, however, are 
not the only cells that die in the deg-1 animals.  A variable number 
of the IL1 neurons die at about the time of hatching as does a cell 
tentatively identified as AVG.  There is also a pair of cells (perhaps 
AVD) that die around the time of the L4 molt.  (In preliminary 
experiments it seems that the temperature-critical periods for these 
deaths also correspond to the observed time of death at 25 C.)
A number of double mutants have been made to learn about the nature 
of the neuronal degeneration caused by deg-1.  Both unc-86(e1416):deg-
1 (no touch cells) and lin-6(e1466):deg-1 (no postembryonic cells - 
including some of the motor neuron targets for PVC) show the Deg 
phenotype of insensitivity in the tail when prodded with the wire.  In 
addition the deg-1 deaths are not affected by ced-3(n717) or prolonged 
by ced-1(e1735) (there actually may be a few more degenerating deaths 
in the ced-3 double).  These data suggest that deg-1 may act 
autonomously, causing neuronal degenerations that are unaffected by 
the ced mutations.