RNAi of
neg-1 caused a robust suppression of the
pos-1 endomesoderm differentiation defect (79%, n = 152). Similarly, the
neg-1(
tm6077) mutation restored endo-mesoderm specification in
pos-1 mutant embryos to 74% (n = 293), suggesting that
neg-1(
tm6077) behaves like a loss-of-function mutation.