Dutcher S K, Hartwell L H
Cell. 1983 May;33(1):203-10. doi: 10.1016/0092-8674(83)90349-5.
Mutations in four nuclear genes, kar1 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 (-/+ X -/+), 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 kar1, 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.
酿酒酵母接合过程中，四个核基因（kar1、cdc4、cdc28和cdc37）发生突变会阻碍或损害核融合。这四个基因中的任何一个发生突变，对于核融合缺陷而言都是隐性的；在两个细胞均为这四个突变中任何一个的杂合子（-/+ × -/+）的二倍体细胞之间进行交配时，核融合能够正常进行。然而，这四个基因中的任何一个发生突变都是“核显性”的；也就是说，为了成功实现核融合，两个亲本核都必须为每个基因贡献一个野生型等位基因。为了区分两种可能解释核显性的模型，我们检测了突变核在经过异核体细胞质后的核融合能力。在这个实验中，kar1、cdc28和cdc37的核融合缺陷在表型上均得到了抑制（cdc4无法进行检测）。我们从结果中得出结论，KAR1、CDC28和CDC37基因产物能够在异核体的核之间扩散，并且它们可能在细胞融合之前就为核融合发挥其功能了。一个与CDC28和CDC37在有丝分裂以及核融合中的作用相一致的简单模型是，这些基因产物是细胞核的结构成分，必须在一个细胞周期内构建到细胞核中，以便在下一个G1期实现成功的核融合。
