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Transcriptome analysis during thermal-induced endogenous mutagenesis in a strict psychrotrophic Aeromonas salmonicida subp. salmonicida strain 严格嗜冷养型沙门氏气单胞菌亚群热诱导内源性突变的转录组。salmonicida压力。
IF 3.4 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-09-01 DOI: 10.1016/j.resmic.2025.104305
Javier Santander , Ahmed Hossain , Katherine Valderrama , Jules Hermet , Trung Cao , Oluwatoyin Onireti , Ignacio Vasquez , Hajarooba Gnanagobal
Aeromonas salmonicida is one of the earliest identified fish pathogens and the causative agent of furunculosis. A. salmonicida can be cultivated at temperatures as high as 30 °C, but at temperatures over 24 °C, insertion sequence (IS) elements cause endogenous mutagenesis. Here, we used a phenotypical and transcriptomics analysis to study the molecular aspects of A. salmonicida endogenous mutagenesis. Endogenous mutagenesis became evident after 12 h post-thermal induction and reached the highest level after 24 h. RNA was extracted from A. salmonicida grown at 15 and 28 °C after 16 h. Differential gene expression analysis showed that 344 differential expressed genes were up-regulated and 364 were down-regulated at 28 °C. Several ISs were upregulated in the chromosome and virulence plasmid. Virulence genes, including the type 3 secretion system, A-layer, and melanin synthesis, were downregulated. Overall, our result indicates that A. salmonicida incubated at 28 °C was under moderate heat stress but under strong stress caused by ISs mutagenesis. These results align with the hypothesis that ISs constrain virulent A. salmonicida to a psychrotrophic lifestyle, potentially transitioning to an attenuated mesophilic lifestyle.
沙门氏菌气单胞菌是最早发现的鱼类病原体之一,也是引起真菌病的病原体。沙门氏菌可在高达30°C的温度下培养,但在超过24°C的温度下,插入序列(IS)元件会引起内源性突变。在这里,我们使用表型和转录组学分析来研究沙门氏菌内源性诱变的分子方面。内源诱变作用在热诱导12 h后开始显现,24 h后达到最高水平。在15℃和28℃培养16 h后提取沙门氏菌RNA。差异基因表达分析显示,28℃条件下差异表达基因上调344个,下调364个。染色体和毒力质粒中多个ISs上调。毒力基因,包括3型分泌系统、a层和黑色素合成下调。总的来说,我们的结果表明,28°C孵育的沙门氏菌处于中等热应激状态,但处于ISs诱变引起的强应激状态。这些结果与假设一致,即ISs将毒性沙门氏菌限制为嗜冷性生活方式,可能过渡到减弱的嗜温性生活方式。
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引用次数: 0
Nutrients drive the antibiotic-specific evolution of resistance in Pseudomonasaeruginosa. 营养物质驱动铜绿假单胞菌耐药性的抗生素特异性进化。
IF 3.4 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-09-01 DOI: 10.1016/j.resmic.2025.104323
Maik Kok, Laura B Zwep, Robert S Jansen, Thomas Hankemeier, J G Coen van Hasselt

Pseudomonas aeruginosa can exploit its metabolic flexibility during cystic fibrosis lung infections to reduce antibiotic sensitivity and offset resistance costs, traits that influence its evolutionary trajectory. Although both traits are linked to nutrient conditions, their role in resistance evolution remains poorly defined. We examined how single-nutrient conditions influence resistance evolution in P. aeruginosa through phenotypic and genotypic adaptations after adaptive laboratory evolution with different antibiotics in single-nutrient media. Antibiotic susceptibility testing showed limited MIC differences for ceftazidime and imipenem, but stronger effects for ciprofloxacin, colistin, and tobramycin. Ciprofloxacin evolution in glutamate medium yielded the highest MIC increase, with at least a 4-fold rise, whereas tobramycin evolution in glucose resulted in up to a 4-fold MIC reduction compared to lineages evolved under all other nutrient conditions for the same antibiotic. Whole-genome sequencing showed nutrient-specific mutation in wbpL after tobramycin evolution in glucose, and fusA and pmrB across conditions. Ciprofloxacin resistance in glutamate-lineages involved yicC, whereas nfxB mutations were absent in glucose- and arginine-evolved lineages. No distinct nutrient-specific differences were seen for colistin. These findings underscore the significant role of nutrient conditions in shaping resistance and highlight the need to consider physiologically relevant media when studying antibiotic resistance evolution.

铜绿假单胞菌可以在囊性纤维化肺部感染期间利用其代谢灵活性来降低抗生素敏感性并抵消耐药性成本,这些特性影响其进化轨迹。尽管这两种性状都与营养条件有关,但它们在抗性进化中的作用仍不明确。我们研究了在单一营养培养基中不同抗生素的适应性实验室进化后,单一营养条件如何通过表型和基因型适应影响铜绿假单胞菌的耐药性进化。抗生素敏感性试验显示头孢他啶和亚胺培南的MIC差异有限,但环丙沙星、粘菌素和妥布霉素的MIC差异更大。环丙沙星在谷氨酸培养基中的进化产生了最高的MIC增加,至少增加了4倍,而妥布霉素在葡萄糖中的进化导致与在所有其他营养条件下进化的谱系相比,相同抗生素的MIC降低了4倍。全基因组测序显示,妥布霉素在葡萄糖、fusA和pmrB中进化后,wbpL发生了营养特异性突变。在谷氨酸谱系中,环丙沙星耐药涉及yicC,而在葡萄糖和精氨酸进化谱系中,不存在nfxB突变。粘菌素没有明显的营养特异性差异。这些发现强调了营养条件在形成耐药性中的重要作用,并强调了在研究抗生素耐药性进化时考虑生理相关介质的必要性。
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引用次数: 0
Multi-drug resistance and diversity of mobile genetic elements in Escherichia coli isolated from migratory bird in Poyang Lake 鄱阳湖候鸟大肠杆菌多药耐药及移动基因多样性分析
IF 3.4 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-09-01 DOI: 10.1016/j.resmic.2025.104306
Haixin Deng , Huiping Liang , Qinghua Zeng , Peng Huang , Hui Yan , Huabin Cao , Huansheng Wu
With the spread of antibiotic resistance genes such as blaCTX-M-2, dfrA1 and blaNDM-1, the problem of drug resistance in E. coli is becoming increasingly serious [1]. This study aimed to identify integrons genes and MGEs in E. coli isolated from migratory birds' feces at Poyang Lake, Jiangxi Province, focusing on their role in antimicrobial resistance (AMR). The 114 isolated E. coli strains were tested by standard disk diffusion method and genetic testing method. Results showed 64.04 % (73/114) of isolates were multi-drug resistance (MDR), mainly resistant to 3–6 antibiotics. Common resistances included neomycin (50 %) and streptomycin (48.25 %). We detected 21 mobile genetic elements, including IS903 (92.11 %), traA (72.81 %), ISCR3 (64.91 %), and ISpa7 (50 %). These elements were present in all isolates, forming 112 combinations. Significant differences in resistance rates were found between class I integron-positive and negative strains for doxycycline, tetracycline, bacitracin, and streptomycin (P < 0.01), and for neomycin (P < 0.05). Class II integron-positive bacteria showed higher resistance to doxycycline (P < 0.01) and ceftizoxime (P < 0.05). No significant differences were observed for class III integron-positive strains. This study underscores the prevalence of multidrug-resistant and the diversity of mobile genetic elements in E. coli, emphasizing the need for continuous monitoring.
随着blaCTX-M-2、dfrA1、blaNDM-1等耐药基因的传播,大肠杆菌的耐药问题日益严重。本研究旨在鉴定江西鄱阳湖候鸟粪便中大肠杆菌的整合子基因和MGEs,重点研究它们在抗菌素耐药性(AMR)中的作用。采用标准圆盘扩散法和基因检测法对114株分离的大肠杆菌进行检测。结果显示,64.04%(73/114)的分离株为多药耐药(MDR),主要对3-6种抗生素耐药;常见的耐药包括新霉素(50%)和链霉素(48.25%)。共检测到21个移动遗传元件,包括IS903(92.11%)、traA(72.81%)、ISCR3(64.91%)和ISpa7(50%)。这些元素在所有分离株中均存在,形成112个组合。I类整合子阳性菌株与阴性菌株对强力霉素、四环素、杆菌霉素和链霉素的耐药率差异有统计学意义(P < 0.01),对新霉素的耐药率差异有统计学意义(P < 0.05)。II类整合子阳性菌对强力霉素(P < 0.01)和头孢替昔肟(P < 0.05)有较高的耐药性。III类整合子阳性菌株间无显著差异。本研究强调了大肠杆菌多重耐药的普遍性和可移动遗传元件的多样性,强调了持续监测的必要性。
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引用次数: 0
Metabolic adaptation via glycolysis and iron acquisition drives Klebsiella pneumoniae–induced intraocular inflammation and visual impairment 通过糖酵解和铁获取的代谢适应驱动肺炎克雷伯菌引起的眼内炎症和视力损害。
IF 3.4 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-09-01 DOI: 10.1016/j.resmic.2025.104321
Ping Lu , Juan Xue , Xuemeng Ji
Klebsiella pneumoniae is a major cause of endogenous endophthalmitis, a rapidly progressing intraocular infection associated with severe inflammation and vision loss. The vitreous body presents a hypoxic and iron-restricted environment, yet the bacterial metabolic adaptations that enable persistence in this niche remain largely unknown. Here, we show that K. pneumoniae undergoes metabolic reprogramming to facilitate intraocular survival, characterized by enhanced glycolysis and siderophore-mediated iron acquisition. Proteomic profiling under vitreous-mimicking conditions revealed significant upregulation of PfkA, PykF, and EntB. Targeted deletion of these genes impaired bacterial growth under hypoxia and iron limitation, and significantly reduced intraocular colonization, proinflammatory cytokine production, and visual impairment in a murine model. Double mutants lacking both glycolytic and iron acquisition pathways were nearly avirulent. Correspondingly, infected eyes exhibited lower levels of lactate and iron, reflecting reduced bacterial metabolic activity. These findings establish glycolysis and iron acquisition as critical determinants of K. pneumoniae virulence in the eye and provide insight into the metabolic strategies underpinning bacterial persistence in nutrient-limited host environments.
肺炎克雷伯菌是内源性眼内炎的主要病因,眼内炎是一种进展迅速的眼内感染,伴有严重炎症和视力丧失。玻璃体呈现出缺氧和限制铁的环境,然而细菌的代谢适应使其能够在这个生态位中持续存在,这在很大程度上仍然是未知的。在这里,我们发现肺炎克雷伯菌经历代谢重编程以促进眼内生存,其特征是糖酵解和铁载体介导的铁获取增强。在玻璃体模拟条件下的蛋白质组学分析显示PfkA、PykF和EntB的显著上调。在小鼠模型中,这些基因的靶向缺失会在缺氧和铁限制下损害细菌的生长,并显著减少眼内定植、促炎细胞因子的产生和视力损害。缺乏糖酵解和铁获取途径的双突变体几乎是无毒的。相应地,受感染的眼睛显示出较低的乳酸和铁水平,反映了细菌代谢活动的减少。这些发现确定了糖酵解和铁获取是肺炎克雷伯菌眼部毒力的关键决定因素,并为在营养有限的宿主环境中支持细菌持久性的代谢策略提供了见解。
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引用次数: 0
Effect of Pseudomonas aeruginosa ExoU on airway epithelial cells through MUC1-C nuclear translocation 铜绿假单胞菌ExoU通过MUC1-C核易位对气道上皮细胞的影响。
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104301
Alexandre Costa Monteiro , Karen Rosalino Emmerick , Lhousseine Touqui , Alessandra Mattos Saliba
The opportunistic pathogen Pseudomonas aeruginosa plays a significant role in hospital-acquired pneumonia, with the secretion of ExoU - a virulence factor expressed by select P. aeruginosa strains - linked to poor clinical outcomes. This is due to ExoU's phospholipase A2 activity, which triggers an uncontrolled inflammatory response, leading to severe pathologies. Here, we delve into ExoU's impact on mucin-1 (MUC1), a critical mucus component with immunomodulatory properties on pulmonary cell surfaces. Our findings reveal that infection of human respiratory epithelial cells by an ExoU-negative P. aeruginosa strain boosts MUC1 expression, yet ExoU secretion by the bacteria diminishes MUC1 mRNA and protein levels through JNK pathway disruption. Interestingly, despite reduced overall cell-associated MUC1 levels, ExoU prompts MUC1 accumulation within the nucleus, where the MUC1 cytoplasmic tail (MUC1-C) may act as a transcriptional coactivator. Notably, treating epithelial respiratory cell cultures with GO-201, a specific MUC1-C inhibitor, diminished CXCL-8 secretion induced by ExoU. In essence, our study highlights how infection by ExoU-producing P. aeruginosa strains suppresses MUC1 expression during infection, while enhancing MUC1-C translocation to the nucleus, where it plays a pro-inflammatory role. This unique mechanism sheds light on how ExoU can impact the host's defense against P. aeruginosa, potentially compromising host health.
机会致病菌铜绿假单胞菌(Pseudomonas aeruginosa)在医院获得性肺炎中起着重要作用,ExoU(一种由特定铜绿假单胞菌菌株表达的毒力因子)的分泌与临床预后不良有关。这是由于ExoU的磷脂酶A2活性,引发不受控制的炎症反应,导致严重的病理。在这里,我们深入研究了ExoU对黏液蛋白-1 (MUC1)的影响,MUC1是一种在肺细胞表面具有免疫调节特性的关键黏液成分。我们的研究结果表明,ExoU阴性的铜绿假单胞菌菌株感染人呼吸道上皮细胞可提高MUC1的表达,但细菌分泌ExoU通过JNK通路破坏降低MUC1 mRNA和蛋白水平。有趣的是,尽管整体细胞相关MUC1水平降低,但ExoU促进了MUC1在细胞核内的积累,其中MUC1细胞质尾部(MUC1- c)可能作为转录辅激活因子。值得注意的是,用特异性MUC1-C抑制剂GO-201处理上皮呼吸细胞培养物,可减少ExoU诱导的CXCL-8分泌。从本质上讲,我们的研究强调了产生exou的铜绿假单胞菌菌株在感染过程中如何抑制MUC1的表达,同时增强MUC1- c向细胞核的易位,在细胞核中发挥促炎作用。这种独特的机制揭示了ExoU如何影响宿主对铜绿假单胞菌的防御,从而潜在地损害宿主的健康。
{"title":"Effect of Pseudomonas aeruginosa ExoU on airway epithelial cells through MUC1-C nuclear translocation","authors":"Alexandre Costa Monteiro ,&nbsp;Karen Rosalino Emmerick ,&nbsp;Lhousseine Touqui ,&nbsp;Alessandra Mattos Saliba","doi":"10.1016/j.resmic.2025.104301","DOIUrl":"10.1016/j.resmic.2025.104301","url":null,"abstract":"<div><div>The opportunistic pathogen <em>Pseudomonas aeruginosa</em> plays a significant role in hospital-acquired pneumonia, with the secretion of ExoU - a virulence factor expressed by select <em>P. aeruginosa</em> strains - linked to poor clinical outcomes. This is due to ExoU's phospholipase A<sub>2</sub> activity, which triggers an uncontrolled inflammatory response, leading to severe pathologies. Here, we delve into ExoU's impact on mucin-1 (MUC1), a critical mucus component with immunomodulatory properties on pulmonary cell surfaces. Our findings reveal that infection of human respiratory epithelial cells by an ExoU-negative <em>P. aeruginosa</em> strain boosts MUC1 expression, yet ExoU secretion by the bacteria diminishes MUC1 mRNA and protein levels through JNK pathway disruption. Interestingly, despite reduced overall cell-associated MUC1 levels, ExoU prompts MUC1 accumulation within the nucleus, where the MUC1 cytoplasmic tail (MUC1-C) may act as a transcriptional coactivator. Notably, treating epithelial respiratory cell cultures with GO-201, a specific MUC1-C inhibitor, diminished CXCL-8 secretion induced by ExoU. In essence, our study highlights how infection by ExoU-producing <em>P. aeruginosa</em> strains suppresses MUC1 expression during infection, while enhancing MUC1-C translocation to the nucleus, where it plays a pro-inflammatory role. This unique mechanism sheds light on how ExoU can impact the host's defense against <em>P. aeruginosa</em>, potentially compromising host health.</div></div>","PeriodicalId":21098,"journal":{"name":"Research in microbiology","volume":"176 5","pages":"Article 104301"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Functional diversity of AI-2/LuxS system in lactic acid bacteria: Impacts on biofilm formation and environmental resilience 乳酸菌AI-2/LuxS系统的功能多样性:对生物膜形成和环境恢复力的影响
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104296
Hopeful Tusalifye Kanthenga , Riza Jane S. Banicod , Wilson Ntege , Moses Njeru Njiru , Aqib Javaid , Nazia Tabassum , Young-Mog Kim , Fazlurrahman Khan
A key component of microbial communication, autoinducer-2 (AI-2) signaling, affects several physiological processes, including environmental adaptation and biofilm formation in lactic acid bacteria (LAB). The multifarious contribution of AI-2, synthesized by LuxS, in improving biofilms and tolerance to hostile conditions in LAB has been investigated in this review. The evolutionary conservation and diversity of AI-2 are shown by a phylogenetic analysis of luxS gene among several LAB species. Furthermore, AI-2 signaling in LAB improves resistance to unfavorable environmental factors, including pH fluctuations, temperature extremes, and antimicrobial agents. Lactic acid bacteria could set off defenses against harmful impacts from environmental stresses.
作为微生物通讯的关键组成部分,自诱导剂-2 (AI-2)信号影响乳酸菌(LAB)的几个生理过程,包括环境适应和生物膜形成。本文综述了由LuxS合成的AI-2在改善LAB生物膜和对恶劣条件的耐受性方面的各种贡献。luxS基因在几个LAB物种间的系统发育分析显示了AI-2的进化保守性和多样性。此外,LAB中的AI-2信号传导提高了对不利环境因素的抗性,包括pH波动、极端温度和抗菌药物。乳酸菌可以防御来自环境压力的有害影响。
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引用次数: 0
2-Chloromethyl anthraquinone inhibits Candida albicans biofilm formation by inhibiting the Ras1-cAMP-Efg1 pathway 2-氯甲基蒽醌通过抑制Ras1-cAMP-Efg1通路抑制白色念珠菌生物膜形成
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104280
Haoying Zhang, Qi Zhang, Ting Zuo, Ziqi Wang, Jianmin Liao, Yuanyuan Lu
Candida albicans is an opportunistic pathogen, and the formation of its biofilm makes it resistant to traditional antifungal therapy. Anthraquinones have universal antibacterial activity. We evaluated the inhibitory effects of 2-chloromethyl anthraquinone on C. albicans adhesion, mycelial morphology transformation, and biofilm formation. The results showed that 2-chloromethyl anthraquinone could inhibit C. albicans adhesion, mycelium formation, and biofilm formation in a dose-dependent manner at 2 μg/mL. In addition, 2-chloromethyl anthraquinone significantly inhibited the expression of biofilm formation-related genes in C. albicans, including ALS1, CPH1, ECE1, HWP1, TEC1, BCR1, and UME6. In addition, Ras1-cAMP-Efg1 pathway-related genes (RAC1, CYR1, and TPK2) were also significantly down-regulated, indicating that the inhibitory effect of 2-chloromethyl anthraquinone on C. albicans biofilms may be related to the Ras1-cAMP-Efg1 signaling pathway. In summary, the results of this study confirmed the inhibitory mechanism of 2-chloromethyl anthraquinone on the virulence factors of C. albicans, which laid a theoretical foundation for its use as an anti-biofilm agent against C. albicans.
白色念珠菌是一种机会性病原体,其生物膜的形成使其对传统的抗真菌治疗具有耐药性。蒽醌类具有普遍的抗菌活性。我们评估了2-氯甲基蒽醌对白色念珠菌粘附、菌丝形态转化和生物膜形成的抑制作用。结果表明,在2 μg/mL浓度下,2-氯甲基蒽醌对白色念珠菌的粘附、菌丝的形成和生物膜的形成均有抑制作用,且呈剂量依赖性。此外,2-氯甲基蒽醌显著抑制白色假体生物膜形成相关基因ALS1、CPH1、ECE1、HWP1、TEC1、BCR1和UME6的表达。此外,Ras1-cAMP-Efg1通路相关基因(RAC1、CYR1、TPK2)也显著下调,说明2-氯甲基蒽醌对白色念珠菌生物膜的抑制作用可能与Ras1-cAMP-Efg1信号通路有关。综上所述,本研究结果证实了2-氯甲基蒽醌对白色念珠菌毒力因子的抑制机制,为其作为抗白色念珠菌生物膜剂的应用奠定了理论基础。
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引用次数: 0
Switching off the yeast-to-hyphae transition in Yarrowia lipolytica through histone deacetylase inhibitors 通过组蛋白去乙酰化酶抑制剂关闭脂性耶氏菌酵母到菌丝的转化。
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104299
Martha Viviana Roa-Cordero , Christian Alfonso Arenas-Sepúlveda , María Cristina Herrera-Plata , Sandra Milena Leal-Pinto , Nubia Andrea Villota-Salazar , Juan Manuel González-Prieto
Fungi can develop a variety of morphotypes to survive, colonize, adapt and prevail under different environmental conditions. In general, two morphological shapes encompass the others: yeast (unicellular) and hyphae (multicellular). Under specific conditions, some fungi can adopt these two cellular morphologies, and for this reason, they are called dimorphic. Histone acetylation and deacetylation are well-known important mechanisms of chromatin remodelling that control cell differentiation processes as dimorphism. The reactions involved are catalysed by histone acetyltransferases (HATs) and histone deacetylases (HDACs), respectively. In the present work, we used Yarrowia lipolytica as a dimorphic fungal model to investigate the effect of HDAC chemical inhibition on the growth and yeast-to-hyphae switch of fungi. For this purpose, we tested the compounds sodium butyrate (SB) and valproic acid (VPA) as epigenetic modulators. Our results indicated that Y. lipolytica tolerates high doses of these inhibitors due to its lipolytic nature. However, once the metabolic capability of the fungus is overcome, SB and VPA strongly suppress hyphal growth, suggesting that histone acetylation plays a pivotal role in the regulation of this process.
真菌可以发展出多种形态,在不同的环境条件下生存、定植、适应和生存。一般来说,两种形态包含其他形态:酵母(单细胞)和菌丝(多细胞)。在特定条件下,有些真菌可以采用这两种细胞形态,因此,它们被称为二态的。组蛋白乙酰化和去乙酰化是众所周知的染色质重塑的重要机制,控制细胞分化过程。所涉及的反应分别由组蛋白乙酰转移酶(HATs)和组蛋白去乙酰化酶(HDACs)催化。本研究以多脂耶氏菌为二态真菌模型,研究了HDAC的化学抑制作用对真菌生长和酵母菌-菌丝转换的影响。为此,我们测试了化合物丁酸钠(SB)和丙戊酸(VPA)作为表观遗传调节剂。我们的研究结果表明,由于其脂溶性,脂溶菌耐受高剂量的这些抑制剂。然而,一旦真菌的代谢能力被克服,SB和VPA强烈抑制菌丝生长,这表明组蛋白乙酰化在这一过程的调节中起关键作用。
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引用次数: 0
MibR and LibR are involved in the transcriptional regulation of the ipdC gene in Azospirillum brasilense Sp7 MibR和LibR参与巴西氮螺旋菌Sp7中ipdC基因的转录调控。
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104295
Sandra R. Reyes-Carmona , Saúl Jijón Moreno , Alberto Ramírez-Mata , María Luisa Xiqui Vázquez , Beatriz Eugenia Baca
Azospirillum brasilense is a PGPR that produces the phytohormone IAA, a signaling molecule involved in bacteria-plant interaction processes. IAA biosynthesis in Azospirillum is mainly carried out via the IPyA pathway in which the enzyme phenylpyruvate decarboxylase encoded by the ipdC gene is the main. The promoter region of ipdC gene contains cis elements that are highly conserved among different Azospirillum strains. In this work, we identified two proteins that interact with the promoter region of the ipdC gene, named MibR and LibR that belong to the MarR and LuxR transcriptional regulators family, respectively. Both proteins have an HTH domain, and in the case of LibR, it has a REC domain, with aspartic acid residue conserved in positions 7, 8 and 54, this last as a possible phosphorylation target. To explore their participation in the regulation of the ipdC gene, mutants of libR, mibR, and libR-mibR double mutant were generated. The results showed a decrease in IAA biosynthesis that was related to the observed decrease in ipdC gene expression mostly in the doble mutant compared with the wild type. In this work we suggest that ipdC transcription is regulated by LibR and MibR, providing new findings insight into the mechanism employed by A. brasilense to control IAA biosynthesis.
Azospirillum brasilense是一种产生植物激素IAA的PGPR, IAA是一种参与细菌-植物相互作用过程的信号分子。氮螺旋藻IAA的生物合成主要通过IPyA途径进行,其中ipdC基因编码的苯丙酮酸脱羧酶是主要途径。ipdC基因启动子区含有在不同氮螺旋菌株间高度保守的顺式元件。在这项工作中,我们鉴定了两种与ipdC基因启动子区域相互作用的蛋白,分别属于MarR和LuxR转录调控家族,称为MibR和LibR。这两种蛋白都有一个HTH结构域,在LibR的情况下,它有一个REC结构域,在位置7,8和54中保留了天冬氨酸残基,这是一个可能的磷酸化目标。为了探索它们在ipdC基因调控中的作用,我们产生了libR、mibR和libR-mibR双突变体。结果表明,与野生型相比,双突变体IAA生物合成的减少主要与ipdC基因表达的减少有关。本研究表明,ipdC转录受到LibR和MibR的调控,为巴西芽孢杆菌控制IAA生物合成的机制提供了新的发现。
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引用次数: 0
Antimicrobial resistance in coagulase negative staphylococci: Genome analysis and role of horizontal gene transfer 凝固酶阴性葡萄球菌的抗菌素耐药性:基因组分析和水平基因转移的作用。
IF 2.5 4区 生物学 Q3 MICROBIOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.resmic.2025.104298
Tansu Dündar, Fatma Köksal Çakırlar
Coagulase-negative staphylococci (CNS) are emerging as significant contributors to antimicrobial resistance, yet their genomic characteristics remain incompletely understood. This study presents a whole-genome analysis of 12 multidrug-resistant CNS strains (Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus hominis) isolated from blood cultures, focusing on antimicrobial resistance genes, mobile genetic elements (MGEs), and horizontal gene transfer (HGT) mechanisms.
We identified 22 resistance genes conferring resistance to 11 antimicrobial classes, many of which were plasmid-associated. Notably, we report the first detection of the ISSha1 insertion sequence in S. hominis, along with novel resistance plasmids, including pGO1 and VRSAp in S. haemolyticus and pAMα1 in S. hominis. The identification of bacteriophage-derived sequences in S. haemolyticus and S. hominis suggests a role for phages in genetic exchange. CRISPR sequences and a Cas gene were detected in S. hominis, suggesting a potential but unconfirmed role in restricting gene transfer. Additionally, pGO1 was identified as a conjugative plasmid, while pAMα1 and VRSAp were determined to be mobilizable, reinforcing the role of CNS in resistance dissemination.
These results highlight CNS as reservoirs of antimicrobial resistance genes and emphasize the importance of species-specific genomic surveillance. Proactive monitoring of CNS is crucial for controlling antimicrobial resistance in clinical settings.
凝固酶阴性葡萄球菌(CNS)正在成为抗菌素耐药性的重要贡献者,但其基因组特征仍不完全清楚。本研究对从血液培养中分离的12株多重耐药CNS菌株(表皮葡萄球菌、溶血葡萄球菌、人型葡萄球菌)进行了全基因组分析,重点研究了耐药基因、移动遗传元件(MGEs)和水平基因转移(HGT)机制。我们鉴定出22个耐药基因,对11种抗菌素具有耐药性,其中许多是质粒相关的。值得注意的是,我们报告了首次在人链球菌中检测到ISSha1插入序列,以及新的耐药质粒,包括溶血链球菌的pGO1和VRSAp,以及人链球菌的pAMα1。溶血链球菌和人血链球菌中噬菌体衍生序列的鉴定表明噬菌体在遗传交换中的作用。在S. hominis中检测到CRISPR序列和一个Cas基因,提示在限制基因转移方面有潜在但未证实的作用。此外,pGO1被鉴定为共轭质粒,而pAMα1和VRSAp被确定为可动员质粒,加强了CNS在抗性传播中的作用。这些结果突出了中枢神经系统作为抗菌素耐药基因的储存库,并强调了物种特异性基因组监测的重要性。主动监测中枢神经系统对于控制临床环境中的抗菌素耐药性至关重要。
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Research in microbiology
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