| pubmed-article:16240118 | pubmed:abstractText | KEM1 is a Saccharomyces cerevisiae gene, conserved in all eukaryotes, whose deletion leads to pleiotropic phenotypes. For the most part, these phenotypes are thought to arise from Kem1p's role in RNA turnover, because Kem1p is a major 5'-3' cytoplasmic exonuclease. For example, the exonuclease-dependent role of Kem1p is involved in the exit from mitosis, by degrading the mRNA of the mitotic cyclin CLB2. Here, we describe the identification of a KEM1 truncation, KEM1(1-975), that accelerated the G1 to S transition and initiation of DNA replication when over-expressed. Interestingly, although this truncated Kem1p lacked exonuclease activity, it could efficiently complement another function affected by the loss of KEM1, microtubule-dependent nuclear migration. Taken together, the results we report here suggest that Kem1p might have a previously unrecognized role at the G1 to S transition, but not through its exonuclease activity. Our findings also support the notion that Kem1p is a multifunctional protein with distinct and separable roles. | lld:pubmed |
