所有的硫转移途径通常都有一个l-半胱氨酸脱硫酶作为共同的初始硫动员酶,作为细胞中许多含硫生物分子的生物合成的硫供体。在大肠杆菌中,内务l-半胱氨酸脱硫酶IscS有几个相互作用的伙伴,它们结合在蛋白质的不同位点。到目前为止,ISCU的交互站点,Fdx,CyaY,和参与铁-硫(Fe-S)簇组装的IscX已被映射,除了Tusa,这是钼辅因子生物合成和mnm5s2U34tRNA修饰所必需的,还有ThiI,参与硫胺素生物合成和s4U8tRNA修饰。先前的研究预测硫受体蛋白一次与IscS结合。大肠杆菌TusA有,然而,被建议参与Fe-S团簇组装,因为在ΔtusA突变体中检测到较少的Fe-S簇。Fe-S团簇含量降低的基础未知。在这项工作中,我们研究了TusA在铁硫簇组装和铁稳态中的作用。我们表明,没有TusA会减少毛皮的翻译,从而导致多效性细胞效应,我们在这项研究中详细剖析。重要铁硫簇是进化上古老的假体群。铁摄取调节剂在控制细菌中铁稳态基因的表达中起主要作用。我们表明,ΔtusA突变体在Fe-S簇的组装中受损并积累铁。Tusa,因此,减少毛皮mRNA翻译,导致多效性细胞效应。
All sulfur transfer pathways have generally a l-cysteine desulfurase as an initial sulfur-mobilizing enzyme in common, which serves as a sulfur donor for the biosynthesis of numerous sulfur-containing biomolecules in the cell. In Escherichia coli, the housekeeping l-cysteine desulfurase IscS has several interaction partners, which bind at different sites of the protein. So far, the interaction sites of IscU, Fdx, CyaY, and IscX involved in iron-sulfur (Fe-S) cluster assembly have been mapped, in addition to TusA, which is required for molybdenum cofactor biosynthesis and mnm5s2U34 tRNA modifications, and ThiI, which is involved in thiamine biosynthesis and s4U8 tRNA modifications. Previous studies predicted that the sulfur acceptor proteins bind to IscS one at a time. E. coli TusA has, however, been suggested to be involved in Fe-S cluster assembly, as fewer Fe-S clusters were detected in a ∆tusA mutant. The basis for this reduction in Fe-S cluster content is unknown. In this work, we investigated the role of TusA in iron-sulfur cluster assembly and iron homeostasis. We show that the absence of TusA reduces the translation of fur, thereby leading to pleiotropic cellular effects, which we dissect in detail in this study.IMPORTANCEIron-sulfur clusters are evolutionarily ancient prosthetic groups. The ferric uptake regulator plays a major role in controlling the expression of iron homeostasis genes in bacteria. We show that a ∆tusA mutant is impaired in the assembly of Fe-S clusters and accumulates iron. TusA, therefore, reduces fur mRNA translation leading to pleiotropic cellular effects.