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对能量保守型甲萘醌:辅酶M-辅酶B异二硫化物还原酶HdrED抑制的转录反应

Transcriptional response of to repression of the energy-conserving methanophenazine: CoM-CoB heterodisulfide reductase enzyme HdrED.

作者信息

Buan Nicole R, Metcalf William W

机构信息

Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.

Department of Microbiology, University of Illinois, Urbana-Champaign, Urbana, Illinois, USA.

出版信息

Microbiol Spectr. 2024 Oct 29;12(12):e0095724. doi: 10.1128/spectrum.00957-24.

DOI:10.1128/spectrum.00957-24
PMID:39472004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11619418/
Abstract

Methane-producing archaea are key organisms in the anaerobic carbon cycle. These organisms, also called methanogens, grow by converting substrate to methane gas in a process called methanogenesis. Previous research showed that the reduction of the terminal electron acceptor is the rate-limiting step in methanogenesis by . In order to gain insight into how the cells sense and respond to the availability of the terminal electron acceptor, we designed an experiment to deplete cells of the essential terminal oxidase enzyme, HdrED. We found that the depletion of HdrED results in a higher abundance of transcripts for methyltransferases (), coenzyme B biosynthesis, C1 metabolism, and pyrimidine compounds. In most cases, these changes were distinct from transcript abundance changes observed during the transition from exponential growth to stationary phase cultures. These data implicate the methylotrophic methanogenesis regulator MsrC (MA4383) in CoM-S-S-CoB heterodisulfide sensing and indicate cells have a specific mechanism to sense intracellular ratio of CoM-S-S-CoB, coenzyme M, and coenzyme B thiols and further suggest transcripts encoding translation and methanogenesis functions are controlled by feed-forward regulation depending on substrate availability.IMPORTANCE is an emerging model archaeon and synthetic biology platform for the production of renewable energy and sustainable chemicals to reduce dependence on petroleum. Research into metabolic networks and gene regulation in this organism and other methanogens will inform genome-scale metabolic modeling and microbial function prediction in uncultured or non-model anaerobes and archaea. This study suggests methanogens use unknown mechanisms to efficiently couple methanogenesis to gene regulation via CoM-S-S-CoB and ATP availability.

摘要

产甲烷古菌是厌氧碳循环中的关键生物。这些生物,也被称为产甲烷菌,通过在一个称为甲烷生成的过程中将底物转化为甲烷气体来生长。先前的研究表明,末端电子受体的还原是产甲烷菌进行甲烷生成的限速步骤。为了深入了解细胞如何感知和响应末端电子受体的可用性,我们设计了一个实验来耗尽细胞中的必需末端氧化酶HdrED。我们发现,HdrED的耗尽导致甲基转移酶、辅酶B生物合成、C1代谢和嘧啶化合物的转录本丰度更高。在大多数情况下,这些变化与从指数生长期到稳定期培养物转变过程中观察到的转录本丰度变化不同。这些数据表明甲基营养型甲烷生成调节因子MsrC(MA4383)参与辅酶M-二硫键-辅酶B异二硫化物的感知,并表明细胞具有一种特定机制来感知细胞内辅酶M-二硫键-辅酶B、辅酶M和辅酶B硫醇的比例,进一步表明编码翻译和甲烷生成功能的转录本受前馈调节的控制,具体取决于底物的可用性。重要性是一种新兴的模式古菌和合成生物学平台,用于生产可再生能源和可持续化学品,以减少对石油的依赖。对这种生物和其他产甲烷菌的代谢网络和基因调控的研究将为未培养或非模式厌氧菌和古菌的基因组规模代谢建模和微生物功能预测提供信息。这项研究表明,产甲烷菌利用未知机制通过辅酶M-二硫键-辅酶B和ATP的可用性有效地将甲烷生成与基因调控联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/a26190798b8e/spectrum.00957-24.f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/2a99d0b99570/spectrum.00957-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/a3b4e550b908/spectrum.00957-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/d37effd21eb9/spectrum.00957-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/89d81b15f1a7/spectrum.00957-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/930acc64dd34/spectrum.00957-24.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/6d7625be6746/spectrum.00957-24.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/d4f55780d14d/spectrum.00957-24.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/be2b51f1b2a9/spectrum.00957-24.f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/a26190798b8e/spectrum.00957-24.f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/2a99d0b99570/spectrum.00957-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/a3b4e550b908/spectrum.00957-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/d37effd21eb9/spectrum.00957-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/89d81b15f1a7/spectrum.00957-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/930acc64dd34/spectrum.00957-24.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/6d7625be6746/spectrum.00957-24.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/d4f55780d14d/spectrum.00957-24.f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/be2b51f1b2a9/spectrum.00957-24.f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2f1/11619418/a26190798b8e/spectrum.00957-24.f009.jpg

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本文引用的文献

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Supplementation of Sulfide or Acetate and 2-Mercaptoethane Sulfonate Restores Growth of the Δ Deletion Mutant during Methylotrophic Methanogenesis.
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