The transcriptional regulator sir-2.1 acts genetically upstream to repress function of ctbp-1 [21]; we predicted that in a sir-2.1 mutant strain, loss of negative regulation of ctbp-1 might result in fast development of AFT. We found that sir-2.1 mutant animals were resistant to ethanol relative to N2, and, while there was a trend toward fast development of AFT, there was not a statistical difference in rate of AFT from N2 (Figure 2). Together, these results suggest that ctbp-1 is a regulator of AFT.
