Worm Breeder's Gazette 7(1): 69
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.
The antimicrotubule drug benomyl strongly affects the growth of C. elegans. Wild-type animals grow slowly and become extremely uncoordinated in the presence of the drug (Chalfie and Thomson, J. Cell Biol., in press). The unc character of the animals correlates with a loss of nerve processes in the ventral cord (Table 1). Interestingly, the drug does not affect the outgrowth of the wild-type touch cells. (The touch cells microtubules have 15 protofilaments; those in the ventral cord cells have 11-protofilaments). However, benomyl does prevent the outgrowth of the touch cells in mec-7 mutants (here the touch cells have 11 protofilaments). Benomyl-resistance has been used to identify alpha-tubulin mutants in Aspergillus (Sheir-Neiss et al., Cell 15: 639-647, 1978). In an attempt to isolate similar mutants in C. elegans, I mutagenized N2 stocks and looked for F2 animals that were non-Unc in the presence of benomyl. Two resistant strains have been isolated so far. The first has a mutation e1880 (ben-1) that maps to the left of linkage group III in the region of mec-12 (from which it is separable). This mutant is dominant, and animals carrying the allele have the normal number of ventral cord processes even in the presence of benomyl (Table 1). The ben-1 mutation also conveys resistance to benomyl for the mec-7 touch cells, i. e. these cells grow out normally in the presence of the drug in the ben-1; No differences have been identified in the tubulin pattern in 2-D gels of ben-1 and wild type. The second mutation-e1881, is weakly semidominant, but has not been fully characterized. Isolation of additional resistant mutants and revertants and characterization of the C. elegans tubulin genes are in progress. [See Figure 1]