Worm Breeder's Gazette 10(3): 149
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.
Three mutations in mec-4 (e1661, u214, and u231) and a single mutation deg-1(u38) result in the degeneration of different sets of neurons. The mec-4 mutations cause the death of the touch cells, and the deg-1 mutation causes the death a number of cells including the IL1 sensory cells and the PVC and AVD interneurons. These mutations are dominant; recessive mutations of these genes do not result in cell death. I have made a number of double mec mutants with the mec-4d to determine whether defects in any other touch gene can affect the touch cell degenerations. John Sulston and I showed in the initial description of the touch mutants (Dev. Biol. 82: 358, 1981) that unc- 86 and mec-3 mutations will prevent the mec-4d deaths. This result demonstrates the specificity of the action of the mec-4 gene, since touch cells are not made in these mutant backgrounds. Mutations in two other touch genes prevent the mec-4d deaths. lin-32 mutations affect the lineages that give rise to the touch cells, so it is not surprising fewer dying cells are seen in the mutants. It was surprising, however, to find that mutations in mec-6 do prevent the mec-4d degenerations. Although all double mutant combinations have not been made, thirteen different mec-6; ave been made using seven of the nine existing mec-6 mutations and all three of the mec-4d mutations. In all cases the mec-6 mutations prevented the touch cell death (because the animals are touch insensitive, the presence of the touch cells was confirmed in young adults by Nomarski observations). One of the mec-6 mutations (u247) is temperature sensitive, and its affect on the degenerations produced by all three mec-4d mutations was also temperature dependent. The cells die at 15 C. Shifting the mutants to 15 C at hatching, however, did not result in the subsequent death of the cells. Either the mec- 4d mutations cannot cause the later death of the touch cells or the suppression caused by the mec-6 mutant product was already irreversible by hatching. The mec-6 mutations (three have been used) also suppress the neuronal deaths caused by the deg-1 mutation. deg-1 mutants do not move when prodded on the tail with a worm pick, but mec-6 and mec-6; do respond when hit with the pick (these animals are still insensitive to the gentler touch of an eyebrow hair). No degenerations are seen in the double mutants (this includes the IL1 cells and other neurons near the nerve ring that usually die in the early L1). Thus, the mec-6 suppression does not exclusively effect cells of the touch circuit. These results indicate that even though the only detectable defect of mec-6 mutants is touch insensitivity, the gene is required for the function of a number of types of nerve cells. mec-6 mutations, thus, suppress the deaths of different sets of nerve cells caused by mutations in two different genes. This finding indicates that there is an underlying molecular similarity in the deaths caused by the mec-4 and deg-1 mutations. mec-6 mutations identify one component that is needed for the degenerative process. The role of mec-6 in this process is not clear. If the mec-4 and deg- 1 mutant products directly cause the degeneration, the mec-6(+) product may be needed to produce functional products from mutant (and, perhaps, wild-type) genes. Alternatively, mec-6 could cause the degenerations, but only when appropriately altered by the action of the mec-4d and deg-1 mutant products. In any case, mec-6 has turned out to be a rather intriguing gene.