The transcription factor CTBP-1 has been shown to bind to and act with the zinc-finger transcription factors PAG-3 and ZAG-1 to repress transcription of target genes [20]. We reasoned that if ctbp-1 mutant animals are defective in AFT because of loss of transcriptional regulation of some effector genes that are cooperatively regulated by these co-repressors, then animals defective in either of the other two co-repressors should also be defective in AFT. Animals mutant in either pag-3 or zag-1 have locomotion defects; we were unable to test zag-1 mutants in our behavioral assays because they are too uncoordinated to allow us to distinguish between locomotion defects induced by ethanol and their baseline uncoordination. The more extreme phenotype of the zag-1 and pag-3 mutants compared with ctbp-1 mutants suggests that those genes have functions in addition to their cooperative role with ctbp-1. 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
