subtle transcriptional dysregulation, which did not meet the criteria for inclusion in that report, may be functionally relevant in the development of AFT. Therefore, we tested whether altering ida-1 function could be an explanation for the altered rate of development of AFT in ctbp-1 and pag-3. We found that the response of the strong loss-of-function ida-1(ok409) mutant animals to ethanol was indistinguishable from that of N2 (Table 1), suggesting that a change in the rate of neurosecretion is not the explanation for the AFT phenotype of animals carrying mutations in these transcriptional regulators. As noted above, we have further observed that pag-3 mutant animals are mildly uncoordinated, while ctbp-1 mutants are not, suggesting that this transcriptional repressor may regulate expression of a larger group of genes than those that overlap with ctbp-1, and ida-1 may be in that class of differentially regulated genes.
