While pag-3 mutant animals are also uncoordinated, their locomotion defect is less severe, and we were able to assess them for the development of AFT. We found that the loss-of-function allele pag-3(n3098) did not develop AFT, and it also suppressed the fast development of AFT of npr-1(ky13) (Figure 1b), suggesting that ctbp-1(eg613) is defective in AFT because it fails to regulate transcription, and that this function of ctbp-1 requires pag-3. Since a mutation in pag-3 was able to suppress the npr-1-mediated fast development of AFT, we reasoned that our genetic screen may have identified an allele of pag-3. Another mutation isolated in our screen, bet16, mapped to the genetic interval containing pag-3 and failed to complement four alleles of pag-3 for the AFT phenotype, as tested in visual assays of speed on ethanol. These results indicate that this behavioral screen identified multiple members of a molecular pathway that is involved in the development of AFT.
