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PHB生物合成可抵消……中的氧化还原应激。 (你提供的原文不完整,“in”后面缺少具体内容)

PHB Biosynthesis Counteracts Redox Stress in .

作者信息

Batista Marcelo B, Teixeira Cícero S, Sfeir Michelle Z T, Alves Luis P S, Valdameri Glaucio, Pedrosa Fabio de Oliveira, Sassaki Guilherme L, Steffens Maria B R, de Souza Emanuel M, Dixon Ray, Müller-Santos Marcelo

机构信息

Department of Biochemistry and Molecular Biology, Universidade Federal do Paraná, Curitiba, Brazil.

Department of Molecular Microbiology, John Innes Centre, Norwich, United Kingdom.

出版信息

Front Microbiol. 2018 Mar 15;9:472. doi: 10.3389/fmicb.2018.00472. eCollection 2018.

DOI:10.3389/fmicb.2018.00472
PMID:29599762
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5862806/
Abstract

The ability of bacteria to produce polyhydroxyalkanoates such as poly(3-hydroxybutyrate) (PHB) enables provision of a carbon storage molecule that can be mobilized under demanding physiological conditions. However, the precise function of PHB in cellular metabolism has not been clearly defined. In order to determine the impact of PHB production on global physiology, we have characterized the properties of a Δ mutant strain of the diazotrophic bacterium . The absence of PHB in the mutant strain not only perturbs redox balance and increases oxidative stress, but also influences the activity of the redox-sensing Fnr transcription regulators, resulting in significant changes in expression of the cytochrome -branch of the electron transport chain. The synthesis of PHB is itself dependent on the Fnr1 and Fnr3 proteins resulting in a cyclic dependency that couples synthesis of PHB with redox regulation. Transcriptional profiling of the Δ mutant reveals that the loss of PHB synthesis affects the expression of many genes, including approximately 30% of the Fnr regulon.

摘要

细菌产生聚羟基链烷酸酯(如聚3-羟基丁酸酯,PHB)的能力,使得其能够提供一种可在严苛生理条件下动用的碳储存分子。然而,PHB在细胞代谢中的精确功能尚未明确界定。为了确定PHB产生对整体生理学的影响,我们已对固氮细菌的Δ突变株特性进行了表征。突变株中PHB的缺失不仅扰乱氧化还原平衡并增加氧化应激,还影响氧化还原感应Fnr转录调节因子的活性,导致电子传递链细胞色素分支的表达发生显著变化。PHB的合成本身依赖于Fnr1和Fnr3蛋白,从而导致一种将PHB合成与氧化还原调节联系起来的循环依赖性。Δ突变株的转录谱分析表明,PHB合成的缺失影响许多基因的表达,包括约30%的Fnr调控子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/6fa05cd5cd2a/fmicb-09-00472-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/12e6c557a76a/fmicb-09-00472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/6e668940505e/fmicb-09-00472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/0dc9f1879b7a/fmicb-09-00472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/7384d4f7ed48/fmicb-09-00472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/d73ad5eacede/fmicb-09-00472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/d15fd40c79b8/fmicb-09-00472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/936f500fedb5/fmicb-09-00472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/6fa05cd5cd2a/fmicb-09-00472-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/12e6c557a76a/fmicb-09-00472-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/6e668940505e/fmicb-09-00472-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/0dc9f1879b7a/fmicb-09-00472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/7384d4f7ed48/fmicb-09-00472-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/d73ad5eacede/fmicb-09-00472-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/d15fd40c79b8/fmicb-09-00472-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/936f500fedb5/fmicb-09-00472-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ef/5862806/6fa05cd5cd2a/fmicb-09-00472-g008.jpg

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