We were interested in determining which genes that are regulated by ctbp-1 and pag-3 are responsible for the defect in AFT that we observed in those animals. To date, in C. elegans, the only specific regulatory target of pag-3 that has been reported is the gene ida-1, which encodes a protein involved in dense core vesicle release. The loss of negative regulation of ida-1 in pag-3 mutants causes increased neurosecretion [22]. We would expect any gene that is important for the shared AFT phenotype in pag-3 and ctbp-1 to also be misregulated in the ctbp-1 mutant. Chen et al. [21] performed microarray analysis of a ctbp-1 mutant, and reported genes with expression differences of 2-fold or more from wild type, and while expression of ida-1 was not reported to be altered in this study, it remained possible that a more 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
