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首页> 外文期刊>Molecular and Cellular Biology >Identification of SLF1 as a new copper homeostasis gene involved in copper sulfide mineralization in Saccharomyces cerevisiae.
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Identification of SLF1 as a new copper homeostasis gene involved in copper sulfide mineralization in Saccharomyces cerevisiae.

机译：鉴定SLF1是新的铜稳态基因，涉及酿酒酵母中的硫化铜矿化。

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In Saccharomyces cerevisiae, at least 12 genes are important for cells to propagate in medium containing elevated concentrations of copper salts (J. Welch, S. Fogel, C. Buchman, and M. Karin, EMBO J. 8:255-260, 1989). Complementation studies were carried out on a copper-sensitive mutation (cup14) from this group. A new yeast gene, designated SLF1, was identified as a multicopy suppressor of the cup14 mutation. Slf1 is important for the physiological process of copper sulfide (CuS) mineralization on the surface of cells cultured in medium containing copper salts. CuS mineralization causes the cells to turn brown. Disruption of SLF1, which is located close to the telomere region of chromosome IV, leads to limited copper sensitivity, and the resulting cells lack the normal brownish coloration when grown in CuSO4-containing medium. Overproduction of Slf1 in wild-type cells confers superresistance to CuSO4 and enhances the coloration of cells cultured in the presence of CuSO4. Upon addition of KCN to Cu-grown cells, the brownish coloration was bleached instantly, and copper ions were solubilized. These data are consistent with Slf1-dependent accumulation of CuS complexes on the cell surface. Disruption of SFL1 also results in loss of the ability of yeast cells to deplete Cu but not Cd ions from the growth medium, whereas overexpression enhances Ca depletion ability and the resulting deposition of CuS particles. It is proposed that Slfl participates in a copper homeostasis pathway, distinct from the Cup1 detoxification system, that leads to sulfide generation and CuS biomineralization on the cell surface. This process may coordinate with the Cup1 pathway at different copper concentrations to prevent copper-induced toxicity.
机译：在酿酒酵母中，至少12个基因对于细胞在含有升高浓度的铜盐的培养基中的繁殖很重要（J. Welch，S. Fogel，C. Buchman，and M. Karin，EMBO J. 8：255-260，1989）。 ）。对来自该组的铜敏感突变（cup14）进行了补充研究。一个新的酵母基因，命名为SLF1，被鉴定为cup14突变的多拷贝抑制剂。 Slf1对于在含有铜盐的培养基中培养的细胞表面上硫化铜（CuS）矿化的生理过程很重要。 CuS矿化导致细胞变成棕色。靠近染色体IV端粒区域的SLF1的破坏导致有限的铜敏感性，并且当在含CuSO4的培养基中生长时，所得细胞缺乏正常的棕褐色。 Slf1在野生型细胞中的过量产生赋予对CuSO4的超抗性，并增强了在CuSO4存在下培养的细胞的着色。将KCN加入到Cu生长的细胞中后，棕色的颜色即刻被漂白，并且铜离子被溶解。这些数据与Slf1依赖的CuS复合物在细胞表面的积累是一致的。 SFL1的破坏还导致酵母细胞从生长培养基中消耗Cu而不是Cd离子的能力丧失，而过表达则增强了Ca的消耗能力，并导致了CuS颗粒的沉积。有人提出，Slfl参与铜稳态代谢途径，这不同于Cup1排毒系统，导致细胞表面产生硫化物和CuS生物矿化。在不同的铜浓度下，此过程可能与Cup1途径协调，以防止铜诱导的毒性。

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