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.