Mutations in four nuclear genes, karl cdc4, 28, and 37, block or impair nuclear fusion during conjugation of Saccharomyces cerevisiae. Mutations in all four genes are recessive for the caryogamy defect; in matings between diploid cells both of which are heterozygous for any one of the four mutations (-/ + × -/+), caryogamy occurs with normal proficiency. However, mutations in all four genes are "nuclear dominant"; that is, both parent nuclei must contribute one wild-type allele of each gene for successful caryogamy. In order to discriminate between two possible models to explain nuclear dominance, we have examined the caryogamy proficiency of mutant nuclei after they had passed through a heterocaryotic cytoplasm. The karl, cdc28, and cdc37 caryogamy defects are all phenotypically suppressed in this experiment (cdc4 could not be tested). We conclude from our results that the KAR1, CDC28, and CDC37 gene products can diffuse between nuclei in a heterocaryon and that they probably perform their function for caryogamy prior to cell fusion. One simple model consistent with the roles of CDC28 and CDC37 in mitosis as well as in caryogamy is that these gene products are structural components of the nucleus that must be built into it during one cell cycle in order to permit successful caryogamy at the next G1.