Worm Breeder's Gazette 11(5): 86

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.

mec-8 Interacts with unc-52 and is Essential for Embryogenesis

R.K. Herman

mec-8 was originally defined by mutations that confer insensitivity 
to light touch, although the mec-8 touch receptor cells are not 
discernibly abnormal (Chalfie and Sulston 1981).  mec-8 mutants are 
fertile but show defects in the fasciculation of amphid dendrites and 
the FITC filling of amphid and phasmid neurons (Perkins et. al.  1986).
Fertile unc-52 mutants show retarded development of body wall muscle 
sarcomeres behind the pharynx (Zengel and Epstein 1980); the myo 
filament lattice detaches progressively from the cell membrane (
Francis and Waterston).  As I reported at the last worm meeting, mec-8 I;
unc-52 II double mutants are synthetic embryonic lethal.  Animals 
homozygous for either mec-8 or unc-52 and carrying a single wild-type 
copy of the other gene are fertile, but the double homozygotes they 
segregate arrest at about the two-fold stage of embryogenesis.  Each 
arrested embryo has an apparently normal pharynx and intestine but a 
variably constricted or lumpy hypodermis; some aspect of elongation, 
which occurs by the circumferential squeezing of the hypodermis (
Priess and Hirsh 1986), appears to be defective.  The synthetic 
lethality is not allele specific: three different mec-8 alleles have 
been tested in various combinations with six different unc-52 alleles, 
and all combinations tested, with one exception, gave the same result. 
The exception was mec-8(u218); 250).  Each of 
these two mutations is temperature sensitive; the double mutant 
exhibited the lumpy embryonic arrest phenotype at 25 C, but was 
fertile at 16 C.  Many other double mutants involving either mec-8 or 
unc-52 (but not both) have been constructed, and all were fertile.
The strong synthetic lethal phenotype suggests that mec-8 and unc-52 
contribute to some common essential function.  Rogalski and Moerman (
WBG 11(3):32) have cloned unc-52 and concluded that it encodes a cell 
adhesion molecule.  The mec-8  fasciculation defect suggests a cell 
adhesion function for mec-8 as well.  Williams and Waterston (WBG 11(1)
:49) have identified lethal alleles of unc-52 that show embryonic 
arrest at the twofold stage.  I have identified two new mec-8 alleles 
that suggest that mec-8 is also essential for embryogenesis.
N2 males were treated with EMS and mated to dpy-5 
8) odites, and F1 progeny 
were screened for touch insensitivity.  Each of the new alleles, mn36 
and mn412, has been outcrossed several times.  Each fails to 
complement mec-8(e398) for touch insensitivity and the FITC staining 
defect.  mn364 homozygotes arrest prior to embryonic elongation; mn412 (
touch insensitive) homozygotes derived from mec-8(+)/mec-8(mn412) 
mothers grow slowly and produce progeny that arrest (somewhat variably)
during embryonic elongation.  For each mutant, the mutation 
responsible for touch insensitivity appears to be inseparable 
recombinationally from the lethality (mn364) or sterility (mn412).  
mn364/mn412 appears to be lethal.