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 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.