Worm Breeder's Gazette 5(2): 24

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.

Growth Inhibition of Acetylcholinesterase Mutants by the Potent Acetylcholinesterase Inhibitor Aldicarb -- Isolation of Resistant Mutants

J. Culotti, G. von Ehrenstein

N2, PR1000 (ace-1), GG202 (ace-2), GG201 (ace-2a, 
8 (ace-2b, n tested 
for growth on NGM plates containing various concentrations of the 
potent acetylcholinesterase inhibitor Aldicarb.  Eggs of all strains 
were able to hatch at the highest concentrations of inhibitor used (.
5mM).  Hatchees subsequently became paralyzed, failed to grow, and 
appeared dead; however, paralysis and growth inhibition were 
reversible even after two days on the inhibitor.  At lower 
concentrations of Aldicarb (.24mM, .11mM, and .04mM) N2 and PR1000 
hatchees survived, grew almost normally, and exhibited uncoordinated 
motion (much heterogeneity), whereas, GG202, GG201, and GG198 hatchees 
were paralyzed, didn't grow in length but did in width, and eventually 
became Dpy.  At .02mM and lower concentrations of Aldicarb, growth and 
motion of all strains was near normal.  Growth inhibition of N2, 
PR1000, and GG202 was exactly paralleled by the Aldicarb sensitivity 
of acetylcholinesterase activity present in these strains.
One hundred forty putative Aldicarb resistant 'revertants' of GG198 
from 35 EMS mutagenized lines were isolated in Gottingen and Evanston. 
Phenotypes include twitchers (3 mutants), curlers (many), paralyzed 
mutants (about 35), and mutants with 'better' motion than GG198 (about 
30).  The high proportion of paras seemed unusual, so we mapped the 
five most defective paras.  Two are approximately 2 map units from dpy-
5 I and failed to complement.  The other three are about 5 map units 
from lon-2 X and haven't been complemented; but all three have an 
uncharacterized effect on male tails.  The musculature of these five 
paras appears normal.  Most of the phenotypic 'revertants' with 
improved motion have not recovered acetylcholinesterase activity.  
Some of these may be 'hyperactives' of the sort turned up in other 
revertant hunts (M.  Chalfie and R.  Horvitz, personal communication)