Worm Breeder's Gazette 12(4): 73 (October 1, 1992)
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 mutants are mechanosensory-defective (Mec) (Chalfie and Au, 1989) and display reduced filling of amphid and phasmid neurons with fluorescent dyes (Dyf), due to improper fasciculation of the ciliated tips of these neurons' processes (Perkins et. al. 1986). As reported before (WBG vol. 12, no.3, 1992), mec-8 also has some role in muscle cell adhesion. Double mutants of mec-8 with viable alleles of unc-52 arrest at the two-fold stage of elongation and are paralyzed (Pat), mimicking the arrest phenotype of stronger unc-52 alleles (B. Williams and R. Waterston). unc-52 encodes a probable component of the basal lamina involved in muscle cell attachment to the hypodermis and cuticle (T. Rogalski and D. Moerman).
We have found that mec-8 mutations alone cause variable defects in body wall muscle, presumably defects in muscle attachment. Surprisingly, this muscle-defective phenotype is cold-sensitive: mec-8 mutants grown at 15°C display muscle defects, whereas those grown at 20°C and 25°C show less severe or no defects. The muscle defects may be responsible for variable late embryonic arrest; early larval arrest (L1-L2) with severe kinks, bulges and improper elongation; and adult morphological abnormalities (Unc, Dpy, kinks, bulges). The stronger alleles analyzed ( u74 and u456 )cause about 20-25% embryonic arrest, 10% larval arrest, and about 5-10% adult abnormalities at 15°C.
We used polarized light microscopy to observe the muscles of defective mec-8 animals. The arrested embryos and larvae show localized detachment of strips of body wall muscle. Bends in the worm correlate to where the muscle has detached. Arrested mup-1 embryos exhibit a similar muscle detachment phenotype (Goh and Bogaert, 1991). Plenefisch and Hedgecock (WBG vol.12, no.3, 1992) have described a number of muscle attachment mutants; one of these, vab-10 ,maps near mec-8 ,but vab-10 and mec-8 seem to complement. Adult mec-8 mutants exhibit disorganized muscle birefringence where there is a kink or bulge, and in the same animal there can be normal-appearing muscle and disorganized muscle. In an area of disorganization, the birefringence is wispy and thinner than the normal muscle strip. Muscle cells at the margins of a disorganized area can appear jumbled and mispositioned
Genetic analysis suggests that the cold-sensitive muscle-defective phenotype, along with the Mec and Dyf phenotypes, is the null state of mec-8 .We have isolated three new EMS-induced alleles of mec-8 in an F1 non-complementation screen; these alleles arose at approximately null frequency (1 in about 3200). All three new mutants are Mec and Dyf, and display embryonic and larval arrests similar to u74 and u456 .Furthermore, the strongest mec-8 alleles, when placed over a deficiency, cause defects similar to the homozygous alleles.
We suggest that mec-8 is involved in attachment of muscle cells and sensory neurons to the hypodermis and cuticle (in the case of touch cell processes and body wall muscle cells) and possibly in the attachment of amphid and phasmid processes to each other.
Perkins et. al. 1986.
Plenefisch and Hedgecock, WBG vol. 12, no.3, 1992.
Goh and Bogaert, 1991.