In order to determine if ctbp-1(eg613) is dependent on a loss of npr-1 function to modify AFT, we crossed the mutation away from the npr-1(ky13) mutation and tested its ability to develop acute tolerance in the presence of wild-type npr-1. When we examined the development of AFT in animals carrying the ctbp-1(eg613) mutation alone, we found that they had reduced AFT compared with N2 animals (Figure 1a), demonstrating that ctbp-1 is a component that is generally required for the development of AFT, independent of the genetic background.
