JOURNAL OF HAZARDOUS MATERIALS
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2020
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IF 9.038
Chang-Mei Li,Hai-Zhen Wu,Yu-Xiao Wang,Shuang Zhu,Chao-Hai Wei
The aim of this work is to study the synergistic effect of Stenotrophomonas sp. N5 and Advenella sp. B9 co-culture (COC) on enhancement of phenol biodegradation. These two strains utilizing phenol as sole carbon and energy source were isolated from phenol-containing coking wastewater. The results of biodegradation experiment showed the COC of N5 and B9 has stronger capability to degrade phenol than either of mono-culture (MOC). Growth kinetics studies indicated inhibitory effect of phenol on COC was reduced by the interaction of N5 and B9 in COC. The RNA-Seq results demonstrated that phenol biodegradation was enhanced by metabolic division of labor (DOL) in COC based on the expression of key genes for phenol degradation. GO enrichment analysis of differentially expressed genes (DEGs) indicated DEGs between COC and MOC degradation systems are mainly concentrated in the synthesis of cell components, microbial growth and metabolism, and catalytic activity. The expression of 3 transcriptional factors (LysR, Two-component system response regulator, and TetR families) which can regulate degradation of aromatic compounds, was identified beneficial to phenol degradation.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
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IF 8.7
Cui-Can Lu,Qing-Song Huang,Wen-Jing Zheng,Xiao-Min Zhao,Tian-Tian Wang,Yan Huang,Jing Wu,Zheng-Fei Yan
BHETase_B exhibited higher activity toward BHET than PET and MHET. • Half-lives of engineered BHETase_B (>5.0 h) was greater than WT at 50 °C. • Mutant Q7I/A106P achieves complete degradation of BHET within 2 h at 50 °C. • Mutant Q7I/A106P plus TurboPETase can synergistically degrade PET. Polyethylene terephthalate (PET) plastic waste poses significant environmental challenges. Enzymatic degradation of PET offers a sustainable recycling route, but intermediate products such as bis (2-hydroxyethyl) terephthalate (BHET) and mono (2-hydroxyethyl) terephthalate (MHET) can inhibit further hydrolysis. A bis (2-hydroxyethyl) terephthalate hydrolase (BHETase_B) from Stenotrophomonas pavanii exhibited hydrolytic activity toward both BHET and MHET, but its poor thermal stability limited industrial application. In this study, a combination of rational design and directed evolution strategies were employed to generate BHETase_B mutants, all of which exhibited significantly improved thermal stability with half-lives greater than 5.0 h at 50 °C, compared to the wild type (<1.5 h). Notably, mutant Q7I/A106P demonstrated a 7.6 °C increase in melting temperature (Tm = 52.5 °C for the wild type) and achieved complete degradation of BHET within 2 h at 50 °C. Mutant Q7I/A106P alone showed limited activity toward solid PET, but significantly enhanced product release when combined with PET hydrolases, especially TurboPETase, releasing 206.1 μM of products, a 1.4-fold increase compared with TurboPETase alone. These findings highlighted the potential of the engineered BHETase_B mutant as a downstream auxiliary enzyme for improving cascade PET degradation. Download: Download high-res image (155KB) Download: Download full-size image
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Journal of Animal Science and Biotechnology
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2023
·Vol. 14
·期 1
·1-17
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IF 7
He Zhaoqi,Zhao Caijun,He Yuhong,Liu Zhuoyu,Fan Guyue,Zhu Kun,Wang Yiqi,Zhang Naisheng,Fu Yunhe,Hu Xiaoyu
Background Mastitis is an inflammatory disease of the mammary gland that has serious economic impacts on the dairy industry and endangers food safety. Our previous study found that the body has a gut/rumen-mammary gland axis and that disturbance of the gut/rumen microbiota could result in ‘gastroenterogenic mastitis’. However, the mechanism has not been fully clarified. Recently, we found that long-term feeding of a high-concentrate diet induced mastitis in dairy cows, and the abundance of Stenotrophomonas maltophilia (S. maltophilia) was significantly increased in both the rumen and milk microbiota. Accordingly, we hypothesized that ‘gastroenterogenic mastitis’ can be induced by the migration of endogenous gut bacteria to the mammary gland. Therefore, this study investigated the mechanism by which enterogenic S. maltophilia induces mastitis.Results First, S. maltophilia was labelled with superfolder GFP and administered to mice via gavage. The results showed that treatment with S. maltophilia promoted the occurrence of mastitis and increased the permeability of the blood-milk barrier, leading to intestinal inflammation and intestinal leakage. Furthermore, tracking of ingested S. maltophilia revealed that S. maltophilia could migrate from the gut to the mammary gland and induce mastitis. Subsequently, mammary gland transcriptome analysis showed that the calcium and AMPK signalling pathways were significantly upregulated in mice treated with S. maltophilia. Then, using mouse mammary epithelial cells (MMECs), we verified that S. maltophilia induces mastitis through activation of the calcium-ROS-AMPK-mTOR-autophagy pathway.Conclusion sIn conclusion, the results showed that enterogenic S. maltophilia could migrate from the gut to the mammary gland via the gut-mammary axis and activate the calcium-ROS-AMPK-mTOR-autophagy pathway to induce mastitis. Targeting the gut-mammary gland axis may also be an effective method to treat mastitis.
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高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Yu Zhang,Zeyuan Li,Shuxin Wei,Changsheng Xu,Minhua Chen,Jierong Sang,Yiru Han,Huang Yan,Zhoukun Li,Zhongli Cui,Xianfeng Ye
Researchers often consider microorganisms from Stenotrophomonas sp. to be beneficial for plants. In this study, the biocidal effects and action mechanisms of volatile organic compounds (VOCs) produced by Stenotrophomonas sp. NAU1697 were investigated. The mycelial growth and spore germination of Fusarium oxysporum f. sp. cucumerinum (FOC), which is a pathogen responsible for cucumber wilt disease, were significantly inhibited by VOCs emitted from NAU1697. Among the VOCs, 33 were identified, 11 of which were investigated for their antifungal properties. Among the tested compounds, 2-ethylhexanol exhibited the highest antifungal activity toward FOC, with a minimum inhibitory volume (MIV) of 3.0 μL/plate (equal to 35.7 mg/L). Damage to the hyphal cell wall and cell membrane integrity caused a decrease in the ergosterol content and a burst of reactive oxygen species (ROS) after 2-ethylhexanol treatment. DNA damage, which is indicative of apoptosis-like cell death, was monitored in 2-ethylhexanol-treated FOC cells by using micro-FTIR analysis. Furthermore, the activities of mitochondrial dehydrogenases and mitochondrial respiratory chain complex III in 2-ethylhexanol-treated FOC cells were significantly decreased. The transcription levels of genes associated with redox reactions and the cell wall integrity (CWI) pathway were significantly upregulated, thus indicating that stress was caused by 2-ethylhexanol. The findings of this research provide a new avenue for the sustainable management of soil-borne plant fungal diseases.
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ENVIRONMENTAL RESEARCH
·
2021
·
IF 6.498
Li Changmei,Wei Gengrui,Wu Haizhen,Wang Yuxiao,Zhu Shuang,Wei Chaohai
Polycyclic aromatic hydrocarbons (PAHs) and phenol are persistent pollutants that coexist in coking wastewater (CWW). Fluoranthene (Flu) is the predominant PAH species in the CWW treatment system. Our work emphasized on distinguishing the effects of phenol on Flu biodegradation by co-culture of Stenotrophomonas sp. N5 and Advenella sp. B9 and illustrated the molecular mechanisms. Results showed Flu biodegradation by co-culture was enhanced by phenol. According to the first-order degradation kinetic analysis of Flu, phenol significantly increased the biodegradation rate constant and shortened the half-life of Flu. Transcriptome analysis pointed out the up-regulation of DNA repair activity and 3717 significantly differentially expressed genes (DEGs), were triggered by 800 mg/L phenol. GO enrichment analysis suggested these DEGs are mainly concentrated in biochemical processes such as metal ion binding and alpha-amino acid biosynthesis, which are closely associated with Flu biodegradation, indicating that phenol promotes DNA repair activity and reduces Flu genotoxicity. qRT-PCR was performed to detect the gene expression of aromatic ring-opening dioxygenase. Combined with transcriptome analysis, the qRT-PCR results suggested phenol did not induce the expression of related PAHs-degrading enzymes. RNA extraction and microbial growth curves of COC and COC + Ph provided further evidence that phenol serves as co-substrate which increases biomass and the concentration of degrading enzymes, therefore promoting the Flu degradation.
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