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.