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Cobalt can fully recover the phenotypes related to zinc deficiency in Salmonella Typhimurium
Metallomics ( IF 3.4 ) Pub Date : 2020-10-22 , DOI: 10.1039/d0mt00145g
Serena Ammendola 1 , Domenico Ciavardelli , Ada Consalvo , Andrea Battistoni
Affiliation  

Cobalt is an essential element for living systems, which, however, make very limited use of this metal, using it mainly in cobalamin-containing enzymes. The reduced use of cobalt compared to other transition metals is generally attributed to the potential toxicity of this element. In this work, we demonstrate that cobalt not only does not have an obvious toxic effect on Salmonella Typhimurium, but that it can efficiently compensate for zinc deficiency in a znuABC deleted strain. In fact, cobalt, but not cobalamin supplementation, rescued all major phenotypic defects of the znuABC strain, including the reduced ability to grow and swim in zinc-deficient media and the high susceptibility to hydrogen peroxide stress. Growth in a cobalt-supplemented defined medium led to the accumulation of large amounts of cobalt both in the wild type and in the znuABC strain. These data suggest that atoms of cobalt may be incorporated in bacterial proteins in place of zinc, ensuring their functionality. In support of this hypothesis we have shown that, in vivo, cobalt can accumulate in ribosomes and replace zinc in a periplasmic Cu,Zn superoxide dismutase (SodCII). Finally, we provide evidence of the ability of cobalt to modulate the intracellular concentration of zinc-regulated proteins (ZnuA, ZinT, and SodCII). Although some observations suggest that in some proteins the replacement of zinc with cobalt can lead to subtle structural changes, the data reported in this study indicate that Salmonella has the ability to use cobalt instead of zinc, without evident harmful effects for cell physiology.

中文翻译:

钴能完全恢复鼠伤寒沙门氏菌缺锌相关表型

钴是生命系统的必需元素,然而,对这种金属的使用非常有限,主要用于含钴胺素的酶。与其他过渡金属相比,钴的使用量减少通常归因于该元素的潜在毒性。在这项工作中,我们证明钴不仅对鼠伤寒沙门氏菌没有明显的毒性作用,而且可以有效地补偿znuABC缺失菌株中的锌缺乏。事实上,钴,而不是钴胺素补充剂,挽救了znuABC 的所有主要表型缺陷应变,包括在缺锌培养基中生长和游泳的能力降低以及对过氧化氢压力的高度敏感性。在补充钴的确定培养基中的生长导致野生型和znuABC菌株中大量钴的积累。这些数据表明,钴原子可以代替锌掺入细菌蛋白质中,从而确保其功能。为了支持这一假设,我们已经证明,在体内, 钴可以在核糖体中积累并在周质 Cu,Zn 超氧化物歧化酶 (SodCII) 中替代锌。最后,我们提供了钴调节锌调节蛋白(ZnuA、ZinT 和 SodCII)细胞内浓度的能力的证据。尽管一些观察结果表明,在某些蛋白质中,用钴替代锌会导致细微的结构变化,但本研究报告的数据表明,沙门氏菌具有使用钴替代锌的能力,而不会对细胞生理产生明显的有害影响。
更新日期:2020-10-22
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