In JOHNSON et al. (1981), the Caenorhabditis elegans mutant strain PR1000, homozygous for the
ace-1 mutation
p1000, is shown to be deficient in the class A subset of acetylcholinesterases, which comprises approximately one-half of the total C. elegans acetylcholinesterase activity. Beginning with this strain, we have isolated 487 new behavioral and morphological mutant strains. Two of these, independently derived, lack approximately 98% of the wild-type acetylcholinesterase activity and share the same specific uncoordinated phenotype; both move forward in a slow and uncoordinated manner, and when mechanically stimulated to induce reversal, both hypercontract and become temporarily paralyzed. In addition to the
ace-1 mutation, both strains also harbor recessive mutations in the same newly identified gene,
ace-2, which maps to chromosome I and is therefore not linked to
ace-1. Gene dosage experiments suggest that
ace-2 is a structural gene for the remaining class B acetylcholinesterases, which are not affected by
ace-1.--The uncoordinated phenotype of the newly isolated, doubly mutant strains depends on both the
ace-1 and
ace-2 mutations; homozygosity for either mutation alone produces normally coordinated animals. This result implies functional overlap of the acetylcholinesterases controlled by
ace-1 and
ace-2, perhaps at common synapses. Consistent with this, light microscopic histochemical staining of permeabilized whole mounts indicates some areas of possible spatial overlap of these acetylcholinesterases (nerve ring, longitudinal nerve cords). In addition, there is at least one area where only
ace-2-controlled acetylcholinesterase activity appears (pharyngeo-intestinal