Bashkirov V I, Solinger J A, Heyer W D
Institute of General Microbiology, University of Bern, Baltzer-Strasse 4, CH-3012 Bern, Switzerland.
Chromosoma. 1995 Nov;104(3):215-22. doi: 10.1007/BF00352186.
The Sep1 (also known as Kem1, Xrn1, Rar5, DST2/Stpbeta) protein of Saccharomyces cerevisiae is an Mr 175,000 multifunctional exonuclease with suspected roles in RNA turnover and in the microtubular cytoskeleton as well as in DNA recombination and DNA replication. The most striking phenotype of SEP1 null mutations is quantitative arrest during meiotic prophase at the pachytene stage. We have constructed a set of N- and C-terminal as well as internal deletions of the large SEP1 gene. Analysis of these deletion mutations on plasmids in a host carrying a null allele (sep1 ) revealed that at least 270 amino acids from the C-terminus of the wild-type protein were dispensable for complementing the slow growth and benomyl hypersensitivity of a null mutant. In contrast, any deletion at the N-terminus abrogated complementing activity for these phenotypes. The sequences essential for function correspond remarkably well with the regions of Sep1 that are homologous to its Schizosaccharomyces pombe counterpart Exo2. In addition, these experiments showed that, despite the high intracellular levels of Sep1, over-expression of this protein above these levels is detrimental to the cell. We discuss the potential cellular roles of the Sep1 protein as a microtubule-nucleic acid interface protein linking its suspected function in the microtubular cytoskeleton with its role as a nucleic acid binding protein.
酿酒酵母的Sep1(也称为Kem1、Xrn1、Rar5、DST2/Stpbeta)蛋白是一种分子量为175,000的多功能核酸外切酶,在RNA周转、微管细胞骨架以及DNA重组和DNA复制中可能发挥作用。SEP1缺失突变最显著的表型是在减数分裂前期粗线期出现数量停滞。我们构建了一组大型SEP1基因的N端、C端以及内部缺失。在携带缺失等位基因(sep1)的宿主中,对质粒上这些缺失突变的分析表明,野生型蛋白C端至少270个氨基酸对于补充缺失突变体的生长缓慢和对苯菌灵超敏性是可有可无的。相反,N端的任何缺失都会消除这些表型的互补活性。功能所必需的序列与Sep1中与其粟酒裂殖酵母对应物Exo2同源的区域非常吻合。此外,这些实验表明,尽管Sep1在细胞内水平较高,但该蛋白在这些水平之上的过表达对细胞是有害的。我们讨论了Sep1蛋白作为微管-核酸界面蛋白的潜在细胞作用,将其在微管细胞骨架中的推测功能与其作为核酸结合蛋白的作用联系起来。