Kitagawa K, Skowyra D, Elledge S J, Harper J W, Hieter P
Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, Canada.
Mol Cell. 1999 Jul;4(1):21-33. doi: 10.1016/s1097-2765(00)80184-7.
We have identified SGT1 as a dosage suppressor of skp1-4, a mutation causing defects in yeast kinetochore function. Sgt1p physically associates with Skp1p in vivo and in vitro. SGT1 is an essential gene, and different sgt1 conditional mutants arrest with either a G1 or G2 DNA content. Genetic and phenotypic analyses of sgt1-3 (G2 allele) mutants support an essential role in kinetochore function. Sgt1p is required for assembling the yeast kinetochore complex, CBF3, via activation of Ctf13p. Sgt1p also associates with SCF (Skp1p/Cdc53p/F box protein) ubiquitin ligase. sgt1-5 (G1 allele) mutants are defective in Sic1p turnover in vivo and Cln1p ubiquitination in vitro. Human SGT1 rescues an sgt1 null mutation, suggesting that the function of SGT1 is conserved in evolution.
我们已确定SGT1是skp1-4的剂量抑制因子,skp1-4是一种导致酵母动粒功能缺陷的突变。Sgt1p在体内和体外均与Skp1p发生物理相互作用。SGT1是一个必需基因,不同的sgt1条件突变体在G1期或G2期DNA含量时停滞生长。对sgt1-3(G2等位基因)突变体的遗传和表型分析支持其在动粒功能中起关键作用。通过激活Ctf13p,Sgt1p是组装酵母动粒复合体CBF3所必需的。Sgt1p还与SCF(Skp1p/Cdc53p/F盒蛋白)泛素连接酶相关。sgt1-5(G1等位基因)突变体在体内Sic1p周转和体外Cln1p泛素化方面存在缺陷。人类SGT1可挽救sgt1缺失突变,这表明SGT1的功能在进化中是保守的。