Worm Breeder's Gazette 4(1): 28
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.
In order to search for additional acetylcholinesterase (AChE) defects, we have isolated approximately 900 morphological and behavioral mutants of C. elegans by EMS mutagenesis of strain P1000 ( ace-1 X mutant strain derived from P-D1 (unc-3 erly called BC46. Using an individual worm radiometric assay to screen these mutants for AChE activity, we have found one mutant, strain G-D44 (ace-2; missing 95%-98% of the AChE activity normally found in P1000. This mutant is slightly uncoordinated, slow moving, and when tapped on the head with a needle, it hypercontracts and releases one or two eggs at a time. A heterozygote derived by crossing G-D44 to N2 males segregated 1/16 UNCs (89/1191) and all of those UNCs assayed (180/180) were missing AChE activity. Similarly, a heterozygote derived by crossing G-D44 to P1000 males segregated 1/4 UNCs (664/2910) and all of those UNCs assayed (105/105) were missing AChE activity. These segregation results suggest that ace-1 and ace-2 are unlinked and that the UNC phenotype arises only when both mutations (ace-1 and ace-2) are homozygous in an individual. A strain homozygous for the ace-2 mutation has been derived and named G202. This strain is nearly wild type in appearance and motion and does not hypercontract or release eggs when tapped with a needle. The ace-2 (G202) mutation is on chromosome I approximately 10 map units from dpy-5. We are currently constructing an ace-2; utant from G202 (ace-2) and P1000 (ace-1) to see if it has the same phenotype as G-D44.