Archer J E, Vega L R, Solomon F
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Cell. 1995 Aug 11;82(3):425-34. doi: 10.1016/0092-8674(95)90431-x.
Genetic configurations resulting in high ratios of beta-tubulin to alpha-tubulin are toxic in S. cerevisiae, causing microtubule disassembly and cell death. We identified three non-tubulin yeast genes that, when overexpressed, rescue cells from excess beta-tubulin. One, RBL2, rescues beta-tubulin lethality as efficiently as does alpha-tubulin. Rbl2p binds to beta-tubulin in vivo. Deficiencies or excesses of either Rbl2p or alpha-tubulin affect microtubule-dependent functions in a parallel fashion. Rbl2p has functional homology with murine cofactor A, a protein important for in vitro assays of beta-tubulin folding. The results suggest that Rbl2p participates in microtubule morphogenesis but not in the assembled polymer.
导致β-微管蛋白与α-微管蛋白比例过高的基因构型在酿酒酵母中具有毒性,会导致微管解聚和细胞死亡。我们鉴定出三个非微管蛋白的酵母基因,当它们过表达时,可使细胞从过量的β-微管蛋白中拯救出来。其中一个基因RBL2拯救β-微管蛋白致死性的效率与α-微管蛋白相同。Rbl2p在体内与β-微管蛋白结合。Rbl2p或α-微管蛋白的缺陷或过量以平行方式影响微管依赖的功能。Rbl2p与鼠辅因子A具有功能同源性,鼠辅因子A是一种对β-微管蛋白折叠体外测定很重要的蛋白质。结果表明,Rbl2p参与微管形态发生,但不参与组装好的聚合物。