Microbiological research最新文献_第7页

Meningitic Escherichia coli disrupts the blood-brain barrier through pyroptosis and tight junction degradation and NLRP6 deficiency aggravates infection outcomes 脑膜炎大肠杆菌通过热亡和紧密连接降解破坏血脑屏障，NLRP6缺乏会加重感染结果

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-11-04 DOI: 10.1016/j.micres.2025.128388

Kaixiang Jia , Yangyang Du , Xinrui Cao , Xin Shen , Jinrong Ran , Yi Lu , Lianci Peng , Zhiwei Li , Rendong Fang

Extraintestinal pathogenic Escherichia coli (ExPEC) can cause meningitis by breaching the blood-brain barrier (BBB), but the underlying mechanisms remain unclear. In this study, we found that meningitic ExPEC disrupts the BBB through two distinct mechanisms: inducing endothelial pyroptotic cell death and disrupting tight junction (TJ) proteins. Transcriptomic analysis revealed activation of cell death pathways and suppression of tight junction signaling in ExPEC-stimulated human cerebral microvascular endothelial cells (hCMEC/D3). ExPEC infection induced pyroptotic cell death characterized by caspase-1 and GSDMD activation, along with inflammatory cytokine production. Additionally, ExPEC reduced TJ protein expression and disrupted their continuous distribution. Based on transcriptomic results showing simultaneous activation of NLR and TLR pathways, we investigated the role of NLRP6, a unique receptor with dual functions. Silencing NLRP6 in hCMECs exacerbated ExPEC-induced TJ protein disruption but reduced pyroptotic cell death. In vivo experiments indicated that NLRP6^-/- mice showed accelerated mortality, higher bacterial loads, more severe brain tissue damage, enhanced TJ protein disruption, and elevated inflammatory cytokines following ExPEC infection. Brain transcriptomic analysis revealed that NLRP6 deficiency resulted in impaired immune function, downregulation of tight junction pathways, and upregulation of neurological dysfunction-related pathways. These results demonstrate that meningitic ExPEC promotes bacterial meningitis through dual BBB disruption mechanisms, and NLRP6 plays a crucial protective role by maintaining BBB integrity during infection.

肠外致病性大肠杆菌（ExPEC）可通过破坏血脑屏障（BBB）引起脑膜炎，但其潜在机制尚不清楚。在这项研究中，我们发现脑膜炎exic通过两种不同的机制破坏血脑屏障：诱导内皮细胞死亡和破坏紧密连接（TJ）蛋白。转录组学分析显示，在u - u刺激的人大脑微血管内皮细胞（hCMEC/D3）中，细胞死亡途径被激活，紧密连接信号被抑制。exic感染可诱导以caspase-1和GSDMD激活为特征的热亡细胞死亡，并伴有炎性细胞因子的产生。此外，ExPEC降低了TJ蛋白的表达，破坏了它们的连续分布。基于NLR和TLR通路同时激活的转录组学结果，我们研究了NLRP6这一具有双重功能的独特受体的作用。在hCMECs中沉默NLRP6加重了eu诱导的TJ蛋白破坏，但减少了热腐细胞死亡。体内实验表明，NLRP6-/-小鼠在ExPEC感染后表现出死亡加速、细菌负荷增加、脑组织损伤更严重、TJ蛋白破坏增强和炎症细胞因子升高。脑转录组学分析显示，NLRP6缺乏导致免疫功能受损，紧密连接通路下调，神经功能障碍相关通路上调。这些结果表明，脑膜炎exic通过双重血脑屏障破坏机制促进细菌性脑膜炎，而NLRP6在感染期间通过维持血脑屏障完整性发挥重要的保护作用。

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引用次数: 0

Microbiome based precision medicine through integrated multiomics and machine learning 结合多组学和机器学习的基于微生物组的精准医学。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-11-03 DOI: 10.1016/j.micres.2025.128384

Abhishek Kumar , Caiming Xu , Tikam Chand Dakal

Gut microbiome (GME) is a dynamic ecosystem composed of diverse microorganisms with extensive functional potential that influence host physiology, endocrinology, and neurology. This review explores how multiomics (m^OMICS) and machine learning (ML) enhance understanding of the GME and its implications for human disease and therapy. Integrating metagenomics, metatranscriptomics, metaproteomics, and metabolomics with ML enables the linkage of microbial composition and function to clinical outcomes. Combined m^OMICS approaches elucidate species and strain dynamics, metabolic pathways, and metabolite production within the gut environment. Techniques such as shotgun metagenomics, metagenome-assembled genomes, and pathway mapping reveal associations between dysbiosis and diseases including inflammatory bowel disease, colorectal cancer, cardiometabolic, and neurological disorders. Mechanistic insights highlight short-chain fatty acids in immune regulation, bile acid transformations in metabolic signaling, and trimethylamine N-oxide in cardiovascular risk. ML models trained on heterogeneous datasets identify disease-related microbial modules, improve patient stratification, and predict therapeutic responses, such as differentiating IBD subtypes and detecting cancer-linked microbial signatures. Network analyses uncover gut microbial interaction patterns influencing host physiology. Emerging integrative tools like MOFA+ , DIABLO, and MintTea strengthen cross-modal analysis and biomarker discovery. Standardized workflows addressing quality control, assembly, binning, annotation, and visualization ensure reproducibility. Together, m^OMICS and ML establish a robust framework for translating GME ecology into clinically relevant biomarkers and precision interventions. To enhance reliability, GME studies should adopt uniform sampling protocols, correct compositional biases, employ interpretable models, and validate findings across multi-site cohorts to advance microbiome-based diagnostics and therapeutics in precision medicine.

肠道微生物组（Gut microbiome， GME）是一个由多种微生物组成的动态生态系统，具有广泛的功能潜力，影响宿主生理、内分泌和神经学。这篇综述探讨了多组学（mOMICS）和机器学习（ML）如何增强对GME的理解及其对人类疾病和治疗的影响。将宏基因组学、亚转录组学、宏蛋白质组学和代谢组学与ML相结合，可以将微生物组成和功能与临床结果联系起来。结合mOMICS方法阐明物种和菌株动力学，代谢途径和肠道环境中的代谢物生产。诸如散弹枪宏基因组学、宏基因组组装基因组和途径制图等技术揭示了生态失调与包括炎症性肠病、结直肠癌、心脏代谢和神经系统疾病在内的疾病之间的关联。机制方面的见解强调了短链脂肪酸在免疫调节中的作用，胆汁酸转化在代谢信号传导中的作用，以及三甲胺n -氧化物在心血管风险中的作用。在异构数据集上训练的ML模型可以识别疾病相关的微生物模块，改善患者分层，并预测治疗反应，例如区分IBD亚型和检测癌症相关的微生物特征。网络分析揭示了影响宿主生理的肠道微生物相互作用模式。新兴的综合工具如MOFA+ 、DIABLO和MintTea加强了跨模态分析和生物标志物的发现。处理质量控制、装配、分组、注释和可视化的标准化工作流确保了再现性。mOMICS和ML共同建立了一个强大的框架，将GME生态学转化为临床相关的生物标志物和精确干预措施。为了提高可靠性，GME研究应采用统一的采样方案，纠正组成偏差，采用可解释的模型，并在多地点队列中验证研究结果，以推进精准医学中基于微生物组的诊断和治疗方法。

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引用次数: 0

mgrB inactivation confers enhanced pathogenicity and immune evasion over mcr-1 expression in colistin-resistant Klebsiella pneumoniae mgrB失活对耐粘菌素肺炎克雷伯菌的致病性和免疫逃避作用强于mcr-1表达。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-11-01 DOI: 10.1016/j.micres.2025.128386

Zhuoren Ling , Ruicheng Zheng , Yanjun Dong , Wenjuan Yin , Lu Qiao , Rong Zhang , Pramod K. Jangir , Qiaoling Sun , Gerald Larrouy-Maumus , Craig MacLean , Yang Wang , Jianzhong Shen , Timothy R. Walsh

Colistin is one of the last treatment options against human infections caused by multi-drug resistant Klebsiella pneumoniae. Colistin resistant K. pneumoniae arises through modifying bacterial lipopolysaccharide (LPS) via two mechanisms: the mgrB inactivation on chromosome and mcr-1 expression - usually plasmid-mediated. Notably, chromosomal-mediated resistance is more common in naturally-occurring clinical K. pneumoniae than plasmid-borne resistance. Herein we demonstrated that K. pneumoniae strain with a mutant mgrB (ΔmgrB) gene exhibited increased pathogenicity compared to those carrying mcr-1, as evidenced in Galleria mellonella and murine bacteraemia model. Strain possessing ΔmgrB showed higher mortality rate, greater bacterial accumulation, and increased damage to host tissue. Although both ΔmgrB and mcr-1 impose fitness cost on K. pneumoniae and enhance bacterial evasion from phagocytosis, ΔmgrB mediated greater bacterial resistance to host defence peptides than mcr-1, providing an evolutionary advantage. These findings indicated distinct features of mgrB-inactivated K. pneumoniae and mcr-1-positive K. pneumoniae in host immunity responses, and promote understanding of how antibiotic-resistant determinants influence host-pathogens interactions.

粘菌素是对抗多重耐药肺炎克雷伯菌引起的人类感染的最后治疗选择之一。耐粘菌素肺炎克雷伯菌是通过修饰细菌脂多糖（LPS）的两种机制产生的：染色体上的mgrB失活和mcr-1的表达-通常是质粒介导的。值得注意的是，在自然发生的临床肺炎克雷伯菌中，染色体介导的耐药性比质粒传播的耐药性更常见。在本文中，我们证明了携带突变mgrB （ΔmgrB）基因的肺炎克雷伯菌株比携带mcr-1的肺炎克雷伯菌株具有更高的致病性，这在mellonella Galleria和小鼠菌血症模型中得到了证明。含有ΔmgrB的菌株显示出更高的死亡率，更大的细菌积聚和对宿主组织的损害增加。虽然ΔmgrB和mcr-1都增加了肺炎克雷伯菌的适应性成本，并增强了细菌对吞噬的逃避，但ΔmgrB介导的细菌对宿主防御肽的抗性比mcr-1更强，这提供了进化优势。这些发现表明mgrb灭活肺炎克雷伯菌和mcr-1阳性肺炎克雷伯菌在宿主免疫反应中的独特特征，并促进了对抗生素耐药决定因素如何影响宿主-病原体相互作用的理解。

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引用次数: 0

Coordinated host resistance and distinct phage strategies shape biofilm-phage dynamics in Pseudomonas aeruginosa 协调宿主耐药性和不同噬菌体策略形成铜绿假单胞菌生物膜-噬菌体动力学。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-11-01 DOI: 10.1016/j.micres.2025.128385

Ganghua Han , Lei Zhao , Ruixin Li , Ruihua Liu , Yingying Wang , Mark Bartlam

Temperate and virulent phages coexist in natural environments and can collaboratively contribute to the lysis of bacterial biofilms. However, their therapeutic potential and the dynamics of phage-biofilm interactions, particularly in clinical contexts, remain poorly understood. In this study, we demonstrated the strong biofilm-lysing capabilities of the temperate phage PaoP1 and virulent phage PaoP5 against Pseudomonas aeruginosa biofilms, highlighting their potential for phage therapy. RNA-seq analysis revealed a shared host resistance mechanism involving the downregulation of flagellar biosynthesis and enhanced biofilm formation. Despite this common host response, the two phages exhibited distinct infection strategies: PaoP1 integrated quiescently into the host genome, while PaoP5 rapidly and abundantly expressed its genes, potentially hijacking the host transcriptional machinery through an as-yet-unknown mechanism. These findings deepen our understanding of phage-biofilm interactions and support the development of phage-based approaches to treat biofilm-associated infections.

温带和强毒噬菌体在自然环境中共存，并能协同促进细菌生物膜的裂解。然而，它们的治疗潜力和噬菌体-生物膜相互作用的动力学，特别是在临床环境中，仍然知之甚少。在这项研究中，我们证明了温带噬菌体PaoP1和强毒噬菌体PaoP5对铜绿假单胞菌生物膜的强生物膜裂解能力，突出了它们在噬菌体治疗方面的潜力。RNA-seq分析揭示了一个共同的宿主抗性机制，包括下调鞭毛生物合成和增强生物膜形成。尽管有这种共同的宿主反应，但这两种噬菌体表现出不同的感染策略：PaoP1静默地整合到宿主基因组中，而PaoP5快速而丰富地表达其基因，可能通过一种尚不清楚的机制劫持宿主的转录机制。这些发现加深了我们对噬菌体-生物膜相互作用的理解，并支持了基于噬菌体治疗生物膜相关感染的方法的发展。

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引用次数: 0

DNA damage-regulated autophagy modulator 1 (DRAM1)-induced lipophagy facilitates Toxoplasma gondii nutrient acquisition and infection DNA损伤调节的自噬调节因子1 （DRAM1）诱导的脂噬促进了弓形虫的营养获取和感染。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-30 DOI: 10.1016/j.micres.2025.128383

Yongheng Hou , Shiguang Huang , Xin-zhuan Su , Fangli Lu

Autophagy is a catabolic process that responds to various environmental stresses, such as nutrient deficiency and intracellular pathogen infection. Toxoplasma gondii is an intracellular parasite that acquires nutrients from the host cells for its proliferation; however, the molecular mechanisms of T. gondii parasites’ nutritional acquisition and metabolism are not fully understood. Here, we found that T. gondii type I RH strain induced host cell autophagy for nutrient acquisition and growth. T. gondii RH strain infection induced DNA damage-regulated autophagy modulator 1 (DRAM1) expression in host cells, and mechanistic analyses suggest an involvement of the IL-33-MyD88-p38/NF-κB signaling pathway in this process. DRAM1 knockdown decreased T. gondii parasite growth, while DRAM1 overexpression increased T. gondii parasite growth by hyperactivating autophagy, especially lipophagy, to provide fatty acids for T. gondii proliferation, which led to increased tissue pathology. This study identified DRAM1 as a critical molecule in regulating type I T. gondii-induced lipophagy, parasite proliferation, and liver pathology in mice. The results provide crucial insights into how T. gondii leverages host autophagy for its gain and identify a target for potential disease management, which may offer new avenues for developing novel drugs against this parasite.

自噬是一种对各种环境胁迫（如营养缺乏和细胞内病原体感染）作出反应的分解代谢过程。刚地弓形虫是一种细胞内寄生虫，从宿主细胞中获取营养以增殖；然而，弓形虫的营养获取和代谢的分子机制尚不完全清楚。在这里，我们发现弓形虫I型RH菌株诱导宿主细胞自噬以获取营养和生长。弓形虫RH感染诱导宿主细胞DNA损伤调节的自噬调节因子1 （DRAM1）表达，机制分析提示IL-33-MyD88-p38/NF-κB信号通路参与了这一过程。DRAM1敲低使弓形虫生长下降，而DRAM1过表达通过过度激活自噬，特别是脂噬，为弓形虫增殖提供脂肪酸，从而促进弓形虫生长，导致组织病理增加。本研究发现，DRAM1是调节小鼠I型弓形虫诱导的脂肪吞噬、寄生虫增殖和肝脏病理的关键分子。这些结果为弓形虫如何利用宿主自噬获得自身利益提供了重要见解，并确定了潜在疾病管理的靶标，这可能为开发针对这种寄生虫的新药提供新的途径。

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引用次数: 0

Dynamic drivers of PAHs transformation in the spatial and temporal continuum of the rhizosphere: An analysis of plant-microbe synergistic mechanism 多环芳烃在根际时空连续体转化的动态驱动因素：植物-微生物协同机制分析。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-29 DOI: 10.1016/j.micres.2025.128380

Jieting Wu , Haoran Yin , Yuxin Li , Lei Zhao , Haijuan Guo , Chengbin Xu , Jing Shang , Xiaofan Fu , Fang Ma , Ruoning Song

The migration and transformation of polycyclic aromatic hydrocarbons (PAHs) in soil systems are inherently constrained by their low solubility, strong sorption affinity to soil particles, and limited bioavailability for biological uptake and degradation. As a critical ecological interface mediating plant-microbe interactions, the rhizosphere plays a pivotal role in facilitating PAHs mobilization and transformation processes. This review systematically examines the spatiotemporal dynamics of PAHs migration and transformation within rhizosphere systems under plant-microbe collaborative regulation, characterized by sequential temporal phases (initial desorption-solubilization, intermediate absorption-accumulation, and terminal degradation-transformation) and spatial stratification (rhizosphere soil-liquid interface, root surface microenvironment, and internal root tissues). We particularly emphasize the synergistic plant-microbe interactions that drive PAHs desorption, solubilization, phytoaccumulation, and biodegradation. Furthermore, we elucidate four potential mechanistic pathways: AHL analogs in root exudates activate bacterial quorum sensing systems to stimulate surfactant production and PAHs-degrading enzyme synthesis; Microbial-derived IAA enhances H⁺ -ATPase activity in plants, facilitating PAHs/H⁺ co-transport mechanisms; Coordinated AHL-IAA signaling promotes Ca²⁺ uptake and upregulates root nodule symbiosis-related gene expression; ROS in root exudates activate bacterial c-di-GMP signaling pathways to enhance microbial colonization and PAHs-degrading enzyme production. We also analyze the practical limitations affecting rhizoremediation efficacy, including climatic conditions, soil heterogeneity, and variations in pollutant types, and propose corresponding future research directions toward the end of the article. This comprehensive analysis establishes a theoretical framework for understanding the mechanistic basis of plant-microbe synergism in rhizospheric PAHs remediation, offering a foundation for advancing rhizosphere engineering and phytoremediation strategies.

多环芳烃（PAHs）在土壤系统中的迁移和转化受到其溶解度低、对土壤颗粒的强吸附亲和力以及生物吸收和降解的生物有效性的限制。根际作为介导植物与微生物相互作用的重要生态界面，在促进多环芳烃的动员和转化过程中起着关键作用。本文系统地研究了植物-微生物协同调控下多环芳烃在根际系统内迁移和转化的时空动态，其特征是时序时间阶段（初始解吸-增溶、中间吸收-积累和最终降解-转化）和空间分层（根际土-液界面、根表面微环境和根内部组织）。我们特别强调协同植物-微生物的相互作用，驱动多环芳烃解吸，增溶，植物积累和生物降解。此外，我们阐明了四种潜在的机制途径：根分泌物中的AHL类似物激活细菌群体感应系统，刺激表面活性剂的产生和多环芳烃降解酶的合成；微生物源IAA增强植物H+ - atp酶活性，促进多环芳烃/H+共转运机制；AHL-IAA信号协调促进Ca2+摄取，上调根瘤共生相关基因表达；根分泌物中的ROS激活细菌c-di-GMP信号通路，促进微生物定植和多环芳烃降解酶的产生。文章最后还分析了影响根茎修复效果的实际限制因素，包括气候条件、土壤异质性和污染物类型的变化，并提出了相应的未来研究方向。这一综合分析为理解根际多环芳烃修复中植物-微生物协同作用的机制基础奠定了理论框架，为推进根际工程和植物修复策略提供了基础。

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引用次数: 0

Circadian rhythm disturbance impairs intestinal mucus barrier and immune microenvironment via sebacic acid-mediated gut dysbiosis 昼夜节律紊乱通过癸二酸介导的肠道生态失调损害肠道粘液屏障和免疫微环境

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-29 DOI: 10.1016/j.micres.2025.128375

Li Cheng , Xinyuan Wang , Qianqian Wang , Kehan Yin, Bo Wang, Biyu Wu, Ping Xu, Hongyi Qiu, Wenjing Ge, Jiali Sun, Qing Shi, Xiujuan Yan , Shengliang Chen

Circadian rhythm disturbance caused by shift work has become increasingly prevalent, emerging as a risk factor for digestive diseases. Both the host’s and the microbial metabolic pathways and functions might be markedly altered by circadian disruption. However, metabolic changes in the gut during shift work are poorly reported. Here, we demonstrated intestinal metabolome signatures in individuals with shift work disorder and identified sebacic acid as a symptoms-related metabolite. Shift work-related circadian rhythm disturbance leads to enhanced hepatic fatty acid ω-oxidation and a significant increase in dicarboxylic fatty acids in feces. Among these, the increased sebacic acid impaired the intestinal mucus barrier by regulating composition of mucus-related gut bacteria, characterized by an increase in Muribaculaceae and a decrease in Akkermansia abundance, along with activated immune system characterized by increased B cell responses, thereby driving the occurrence of intestinal inflammation. The application of the inhibitor for CYP4A, a key ω-hydroxylase in fatty acid oxidation, effectively improved intestinal dysfunction caused by circadian rhythm disturbance. Our findings provide a deep insight into understanding the role of circadian rhythm in maintaining intestinal homeostasis.

轮班工作引起的昼夜节律紊乱越来越普遍，成为消化系统疾病的一个危险因素。昼夜节律紊乱可能显著改变宿主和微生物的代谢途径和功能。然而，轮班工作期间肠道代谢变化的报道很少。在这里，我们展示了轮班工作障碍个体的肠道代谢组特征，并确定了癸二酸是一种与症状相关的代谢物。与轮班工作相关的昼夜节律紊乱导致肝脏脂肪酸ω-氧化增强，粪便中二羧酸显著增加。其中，脂二酸的增加通过调节与黏液相关的肠道细菌组成，导致Muribaculaceae增加，Akkermansia丰度减少，以及以B细胞反应增加为特征的免疫系统激活，从而导致肠道炎症的发生，从而破坏肠道黏液屏障。脂肪酸氧化关键ω-羟化酶CYP4A抑制剂的应用，有效改善了昼夜节律紊乱引起的肠道功能障碍。我们的研究结果为理解昼夜节律在维持肠道内稳态中的作用提供了深入的见解。

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引用次数: 0

Rhizosphere resilience: Exploring microbial diversity and metabolic responses in long-term eucalyptus plantations 根际恢复力：探索长期桉树人工林微生物多样性和代谢反应

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-28 DOI: 10.1016/j.micres.2025.128381

Ning Li , Yuemei Zhang , Zhaolei Qu , Jie Xu , Angang Ming , Hui Sun , Lin Huang

The large-scale cultivation of eucalyptus has led to significant ecological challenges, such as declines in soil microbial diversity and soil degradation. To address these issues, management practices incorporating nitrogen-fixing species and adjusted rotation periods have been proposed. However, their impacts on rhizosphere soil microorganisms and metabolites remain insufficiently understood. This study employed metagenomic and untargeted metabolomics techniques to investigate the response of rhizosphere microorganisms and metabolites in eucalyptus plantations under different management regimes: monoculture plantation, plantation mixed with a nitrogen-fixing tree species, monoculture second-generation plantation, and second-generation mixed plantation. The results revealed that mixed plantation increased microbial diversity compared to continuous cropping. In contrast, second-generation monoculture led to a loss of unique microbial species and reduced microbial community stability compared to the first-generation monoculture. In nutrient-poor pure second-generation plantations, the bacterium Gemmatimonadetes (relative abundance: PF: 0.13 %, PS: 0.39 %, MF: 0.14 %, MS: 0.21 %)—which plays a key role in soil phosphorus cycle—was enriched. Although continuous cropping improved the organic phosphorus mineralization function, it decreased the abundance of genes related to carbon (rbcL and ppc) and phosphorus cycle (phoP and ppk2). The metabolite fluocinolone is negatively correlated with carbon, nitrogen and phosphorus cycle gene components in our dataset, while echinocystic acid and bezitramide are positively correlated. These findings highlight that mixed plantations enhance the ecological niche of eucalyptus rhizosphere by altering the interaction between rhizosphere microbial composition, function, and host plant metabolism.

桉树的大规模种植带来了土壤微生物多样性下降和土壤退化等重大生态挑战。为了解决这些问题，提出了结合固氮物种和调整轮作周期的管理措施。然而，它们对根际土壤微生物和代谢物的影响尚不清楚。本研究采用宏基因组学和非靶向代谢组学技术，研究了桉树人工林在不同管理制度下根际微生物和代谢物的响应：单一栽培、混合固氮树种、单一栽培二代人工林和二代混交林。结果表明，混作比连作增加了土壤微生物多样性。相比之下，与第一代相比，第二代单一栽培导致了独特微生物物种的丧失和微生物群落稳定性的降低。在养分贫乏的纯二代人工林中，对土壤磷循环起关键作用的细菌（相对丰度：PF: 0.13 %,PS: 0.39 %,MF: 0.14 %,MS: 0.21 %）得到了富集。连作虽然提高了有机磷矿化功能，但降低了碳（rbcL和ppc）和磷循环（phoP和ppk2）相关基因的丰度。代谢物氟西诺酮与碳、氮、磷循环基因组分呈负相关，而棘囊酸与bezitramide呈正相关。这些结果表明，混交林通过改变根际微生物组成、功能和寄主植物代谢之间的相互作用，增强了桉树根际生态位。

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引用次数: 0

The interplay between glucose and aromatic compound regulation by two IclR-type transcription factors, LigR1 and LigR2, in Pseudomonas putida KT2440 两个iclr型转录因子LigR1和LigR2在恶臭假单胞菌KT2440中调控葡萄糖和芳香化合物的相互作用

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-28 DOI: 10.1016/j.micres.2025.128382

Elina Kadriu, Sophie Qin, Stephanie M. Prezioso, Dinesh Christendat

Carbon utilization strategies are fundamental to microbial proliferation within complex ecosystems like the soil microbiome. These strategies dictate how microbes prioritize, and metabolize available carbon compounds, shaping community dynamics and ecological outcomes. Pseudomonas putida KT2440, a soil bacterium renowned for its metabolic versatility, exemplifies this adaptive capacity. However, the regulatory mechanism it employs to prioritize sugars vs aromatic compounds for their energy requirement remains poorly understood. Here, we investigated two IclR-type transcriptional regulators, LigR1 and LigR2, which control expression of the lig1 and lig2 operons. Functional analyses reveal that LigR1 and LigR2 activate lig1 but repress the lig2 operon. 4-hydroxybenzoate binding to LigR1 represses gene expression, whereas quinate, protocatechuate, and 4-hydroxybenzoate bind to LigR2 to induce lig2 operon expression. Additionally, ligR1 deletion causes growth defects on glucose and 4-hydroxybenzoate, accompanied by cell elongation and aggregation. We propose that the lig1 operon mediates dual influx of glucose and aromatics via its major facilitator superfamily transporter, while the lig2 operon catalyzes aromatic breakdown through a protocatechuate intermediate and meta-cleavage pathway, supplying oxaloacetate to the TCA cycle. Importantly, P. putida prioritizes shikimate pathway intermediates as energy sources under specific metabolic conditions, such as their accumulation. Overall, these findings redefine the metabolic flexibility of soil pseudomonads and reveal a novel mechanism for thriving in chemically diverse environments. By illuminating a dual regulatory system, our study offers new insight into microbial carbon flux and on the traditional biosynthetic paradigm of the shikimate pathway, revealing its unexpected role in supplying the organism with energy generating compounds.

碳利用策略是土壤微生物群等复杂生态系统中微生物增殖的基础。这些策略决定了微生物如何优先考虑和代谢可用的碳化合物，塑造群落动态和生态结果。恶臭假单胞菌KT2440是一种以其代谢多样性而闻名的土壤细菌，它体现了这种适应能力。然而，它用来区分糖和芳香族化合物的能量需求的调节机制仍然知之甚少。在这里，我们研究了两个iclr型转录调控因子，LigR1和LigR2，它们控制lig1和lig2操纵子的表达。功能分析表明，LigR1和LigR2激活了lig1而抑制了lig2操纵子。4-羟基苯甲酸盐与LigR1结合抑制基因表达，而醌酸盐、原儿茶酸盐和4-羟基苯甲酸盐与LigR2结合诱导lig2操纵子表达。此外，ligR1缺失导致葡萄糖和4-羟基苯甲酸盐上的生长缺陷，并伴有细胞伸长和聚集。我们提出，lig1操纵子通过其主要的促进剂超家族转运体介导葡萄糖和芳香烃的双重内流，而lig2操纵子通过原儿茶酸中间和元裂解途径催化芳香烃的分解，为TCA循环提供草酰乙酸。重要的是，在特定的代谢条件下，如它们的积累，恶臭杆菌优先考虑莽草酸途径中间体作为能量来源。总的来说，这些发现重新定义了土壤假单胞菌的代谢灵活性，并揭示了在化学多样性环境中茁壮成长的新机制。通过阐明双重调控系统，我们的研究为微生物碳通量和莽草酸途径的传统生物合成范式提供了新的见解，揭示了它在为生物体提供能量生成化合物方面的意想不到的作用。

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引用次数: 0

Evolution of Listeria monocytogenes to a strong biofilm producer via the overexpression of Lmo1799 单核增生李斯特菌通过Lmo1799的过表达向强生物膜生产者的进化。

IF 6.9 1区生物学 Q1 MICROBIOLOGY

Microbiological research

Pub Date : 2025-10-27 DOI: 10.1016/j.micres.2025.128379

Alberto Bombelli , Natalia Crespo Tapia , Marcel H. Tempelaars , Sjef Boeren , Heidy M.W. den Besten , Tjakko Abee , Yue Liu

Biofilm formation is key in Listeria monocytogenes’ transmission and persistence in food processing environments. To further understand the mechanisms contributing to biofilm formation, an experimental evolution system was used to isolate strong biofilm producing strains of L. monocytogenes EGDe (reference strain) and FBR16 (hypermutator food isolate). After cycles of plastic surface colonisation, biofilm formation, dispersal and attachment to new surfaces, evolved variants (EV) strains were isolated and found to produce up to seven-fold more biofilm than their respective ancestral (AN) strains. Phenotypic assays revealed an increase in cell surface hydrophobicity as a shared dominant feature of EGDe and FBR16 EV isolates. Proteomic analysis showed proteins Lmo1798, a predicted glucosyltransferase, and Lmo1799, a putative peptidoglycan binding protein with 226 Ala-Asp tandem repeats, to be the most upregulated proteins in both EV strains compared to the AN strains. Genomic analysis of the EGDe EV strain identified a single-nucleotide insertion in the upstream region of lmo1799 and an in-frame deletion of 42 nucleotides in lmo1799, conceivably resulting in high-level expression of a functional protein with 219 Ala-Asp repeats. To evaluate the impact of Lmo1799 on the EV phenotypes and the overall biofilm capacity of L. monocytogenes, EGDe EV mutants lacking lmo1799 and/or the upstream insertion were constructed. Notably, both constructed mutants showed reduced biofilm formation and lower surface hydrophobicity compared to the EV strain, indicating the importance of these mutations for the strong biofilm capacity. Overall, these observations indicate a critical role of Lmo1799 in L. monocytogenes cell surface characteristics and biofilm formation.

生物膜的形成是单核增生李斯特菌在食品加工环境中传播和持续的关键。为了进一步了解生物膜形成的机制，我们利用实验进化系统分离了单核增生乳杆菌EGDe（参比菌株）和FBR16（超突变食品分离物）两株强生膜菌株。经过塑料表面定植、生物膜形成、扩散和附着到新表面的循环，分离出进化变体（EV）菌株，发现其产生的生物膜比各自的祖先（AN）菌株多7倍。表型分析显示，EGDe和FBR16 EV分离株的细胞表面疏水性增加是一个共同的显性特征。蛋白质组学分析显示，与AN菌株相比，预测的糖基转移酶Lmo1798和推测的肽聚糖结合蛋白Lmo1799是两株EV菌株中上调幅度最大的蛋白。对EGDe EV菌株的基因组分析发现，lmo1799上游区域有一个单核苷酸插入，lmo1799帧内缺失42个核苷酸，这可能导致具有219个Ala-Asp重复序列的功能蛋白的高水平表达。为了评估Lmo1799对单核增生乳杆菌EV表型和整体生物膜容量的影响，构建了缺乏Lmo1799和/或上游插入的EGDe EV突变体。值得注意的是，与EV菌株相比，这两种构建的突变体都显示出生物膜形成减少和表面疏水性降低，这表明这些突变对强生物膜能力的重要性。总之，这些观察结果表明Lmo1799在单核增生乳杆菌的细胞表面特征和生物膜形成中起着关键作用。

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引用次数: 0