Hi all,
About three years ago there was a similar thread named “Aldicarb hypersensitivity” but some of the questions didn’t get an answer so I’ll try to revive the theme.
Basically, I’m looking for suggestions as how to interpret hypersensitivity to aldicarb AND levamisole.
There are several examples of mutants that are resistant to both drugs, but I haven’t been able to find papers on mutants that show increased sensitivity to both.
Many thanks in advance,
Peter
Hi,
perhaps this might be useful?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787625/
acr-2(n2420gf) mutants appear to be what you are looking for.
Steve
Thanks Steve - indeed very useful.
Ref 24 in the paper you suggest also list several cases of hypersensitivity to both drugs = more food for thought 
Vashlishan A. B, Madison J. M, Dybbs M, Bai J, Sieburth D, et al. An RNAi screen identifies genes that regulate GABA synapses. Neuron. 2008;58:346–361.
http://www.cell.com/neuron/abstract/S0896-6273(08)00173-6?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627308001736%3Fshowall%3Dtrue
Cheers,
Peter
Here’s a question that is related: Are there examples of mutants that act wild-type in the presence of Aldicarb but are Levamisole hypersensitive? I’m having trouble thinking of an example. Its hard for me to understand how a phenotype like that could arise, but its here staring me in the face.
Via Textpresso:
Hu, Pawson, and Steven:
unc-73 RhoGEF-2 mutants and rab-2 mutants both were weakly resistant to aldicarb and were hypersensitive to the acetylcholine receptor agonist levamisoleI haven’t looked at the rest of the paper to see what else they mention acting similarly, let alone figured out quite what “weakly resistant” means, but it seems likely that “weakly resistant” might be read as acting wild-type.
Aldicarbhttp://www.bocsci.com/description.asp?cas=116-06-3&cid=84 as a cholinesterase inhibitor prevents the breakdown of acetylcholine
in the synapse. The issue that mutants are resistant to aldicarb should be addressed.