Previously we reported the occurrence of 16 linked conidial longevity determinant genes in Neurospora. Mutations of those genes are characterized by a reduction of longevity, a pleiotropic morphological defect, and deficiency of five antioxygenic enzymes. On the basis of the linkage and biochemical data, it was proposed that the genes are spatially and functionally redundant. The results of the present investigation support the hypothesis of functional redundancy. All of the mutants examined were dominant to wild type and failed to complement in heterokaryons. These results are discussed in terms of two molecular models of gene function.