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TusA is a versatile protein that links sulfur mobilization to iron homeostasis and translational efficiency in Escherichia coli

Subject Area Biochemistry
Term from 2014 to 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 262101759
 
Final Report Year 2024

Final Report Abstract

Iron is important for many biological processes, including the TCA cycle, DNA biosynthesis, nitrogen fixation, electron transport and respiration. Due to both its essentiality and high reactivity, the intracellular iron concentration must be strictly regulated in the cell. In E. coli, the ferric uptake regulator (Fur) is mainly responsible to fine tune the iron homeostasis. Our studies show that the deletion of the tusA gene reduced and retarded the translation of the Fur protein, due to the lack of a specific tRNA thiolation controlling translation accuracy. This leads to iron accumulation in the cell and, together with a complex mis-regulation of transcription factors, small RNAs and modulators (as FNR, cAMP-CRP, ErpA, RyhB, FnrS, IscR, CyaY), this causes the reduction of Fe-S clusters assembled by the ISC and SUF systems. ISC and SUF systems are the two main Fe-S cluster assembly machineries in E. coli and both systems mobilise the sulfur through L-cysteine desulfurases, IscS and SufS respectively. While SUF system is limited to the production of Fe-S clusters mainly under oxidative stress and ironlimiting conditions, the ISC system is active under house-keeping and iron-rich conditions. The L-cysteine desulfurase IscS has a central role as sulfur donor for the biosynthesis of numerous sulfur-containing biomolecules by interacting with multiple partner proteins, which bind at different sites one at a time. In addition to TusA, IscS interacts with IscU, CyaY, Fdx and IscX, involved in iron sulfur (Fe-S) cluster assembly, or with ThiI, involved in the biosynthesis of thiamine and s4U8 tRNA modifications. The preference of IscS for a specific interaction partner determines consequentially the direction taken by the sulfur for the respective biosynthesis pathway. In our study we show that TusA is able to partially displace IscU from IscS thereby forming IscS-TusA-IscU heterocomplexes. In this heterocomplex, TusA affects the L-cysteine desulfurase activity of IscS and redirects the sulfur flow towards Moco biosynthesis and tRNA thiolation rather than Fe-S cluster assembly. Furthermore, TusA can completely displace CyaY from its complex with IscS. CyaY is the frataxin homolog of E. coli and its negative modulating effect on the formation of Fe-S cluster by ISC system has been extensively studied. In our work, the possibility if the displaced CyaY can interact with the second L-cysteine desulfurase SufS was investigated. The results indicate that CyaY is able to interact with SufS, alone or with the SufSE complex thereby drastically reducing its activity in vitro. The overexpression of CyaY in vivo has the effect of reducing the L-cysteine desulfurase activity of both IscS and SufS, under different growth conditions.

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