Abstract:
Extracellular cytochrome filaments are proposed to serve as conduits for long-range extracellular electron transfer. The primary functional physiological evidence has been the reported inhibition of Geobacter sulfurreducens Fe(III) oxide reduction when the gene for the filament-forming cytochrome OmcS is deleted. Here we report that the OmcS-deficient strain from that original report reduces Fe(III) oxide as well as the wild-type, as does a triple mutant in which the genes for the other known filament-forming cytochromes were also deleted. The triple cytochrome mutant displayed filaments with the same 3 nm diameter morphology and conductance as those produced by Escherichia coli heterologously expressing the G. sulfurreducens PilA pilin gene. Fe(III) oxide reduction was inhibited when the pilin gene in cytochrome-deficient mutants was modified to yield poorly conductive 3 nm diameter filaments. The results are consistent with the concept that 3 nm diameter electrically conductive pili (e-pili) are required for G. sulfurreducens long-range extracellular electron transfer. In contrast, rigorous physiological functional evidence is lacking for cytochrome filaments serving as conduits for long-range electron transport.
OBJECTIVE: Unraveling microbial extracellular electron transfer mechanisms has profound implications for environmental processes and advancing biological applications. This study on Geobacter sulfurreducens challenges prevailing beliefs on cytochrome filaments as crucial components thought to facilitate long-range electron transport. The discovery of an OmcS-deficient strain\'s unexpected effectiveness in Fe(III) oxide reduction prompted a reevaluation of the key conduits for extracellular electron transfer. By exploring the impact of genetic modifications on G. sulfurreducens\' performance, this research sheds light on the importance of 3-nm diameter electrically conductive pili in Fe(III) oxide reduction. Reassessing these mechanisms is essential for uncovering the true drivers of extracellular electron transfer in microbial systems, offering insights that could revolutionize applications across diverse fields.
摘要:
建议将细胞外细胞色素丝用作远程细胞外电子转移的导管。主要的功能生理证据是,当细丝形成细胞色素OmcS的基因缺失时,有报道抑制了硫化Geobacter还原Fe(III)氧化物的还原。在这里,我们报告了原始报告中的OmcS缺陷菌株减少了Fe(III)氧化物以及野生型,三重突变体也是如此,其中其他已知的细丝形成细胞色素的基因也被删除。三重细胞色素突变体显示的细丝具有与异源表达G.sulfulreducensPilA菌毛蛋白基因的大肠杆菌相同的3nm直径形态和电导。当修饰细胞色素缺陷型突变体中的菌毛蛋白基因以产生导电性差的3nm直径细丝时,Fe(III)氧化物的还原受到抑制。结果与以下概念一致:S.硫还原长距离细胞外电子转移需要3nm直径的导电菌毛(e-pili)。相比之下,缺乏严格的生理功能证据来证明细胞色素丝可以作为远距离电子传递的管道。
目的:揭示微生物胞外电子转移机制对环境过程和推进生物应用具有深远的意义。这项关于硫化Geobacter的研究降低了对细胞色素细丝的普遍信念,因为细胞色素细丝被认为是促进远程电子传输的关键成分。OmcS缺陷菌株在Fe(III)氧化物还原中的意外效果的发现促使对细胞外电子转移的关键管道进行了重新评估。通过探索遗传修饰对G.硫还原性能的影响,这项研究揭示了3nm直径的导电菌毛在Fe(III)氧化物还原中的重要性。重新评估这些机制对于揭示微生物系统中细胞外电子转移的真正驱动因素至关重要。提供可以彻底改变跨不同领域的应用程序的见解。