本次介绍的是《Science Advances》期刊和《Nature Microbiology》期刊的2025年11-12月刊，共11篇文章。
1
标题：
Gut microbial-derived indole-3-propionate improves cognitive function in Alzheimer's disease
肠道微生物来源的吲哚-3-丙酸酯能改善阿尔茨海默病患者的认知功能
作者：
Ling Li, Mengzhen Jia, Cong Yang, Yihang Zhao, Jun Hu, Yu Zhao, Xinyu Hu, Fangjie Ning, Chen Ding, Qingyuan Li, Jun Gong, Xiaoran Jia, Kun Xu, Yuhao Wang, Shuang Zhou, Lu Deng, Lin Shi, Xuhui Chen*, Xuebo Liu*, Zhigang Liu*
链接：
https://pmc.ncbi.nlm.nih.gov/articles/PMC12662223
摘要：
Intermittent fasting (IF) offers a potential strategy to counteract Alzheimer's disease (AD) progression. In our 16-week study on AD transgenic mice, IF positively affected cognitive function and reduced amyloid-β (Aβ) accumulation, verifying the IF's role in modulating neuroinflammation. Multiomics integration revealed strong links between IF-induced hippocampal gene expression, gut microbiota, and serum metabolites beneficial for cognition. Indole-3-propionic acid (IPA) emerged as a pivotal microbial metabolite. Blocking its neuronal receptor, pregnane X receptor (PXR), abolished IF's effects. Human data paralleled these findings, showing lower IPA levels in patients with mild cognitive impairment and AD than in controls. IPA supplementation and IPA-producing Clostridium sporogenes reproduced IF's cognitive benefits, whereas PXR blockade in neurons or disruption of IPA synthesis abrogated them. IPA crossed the blood-brain barrier, exhibited potent anti-inflammatory activity, and suppressed Aβ accumulation, essential for neuroprotection. These results underscore microbial metabolites regulated by IF, particularly IPA, as therapeutic candidates for AD, highlighting the critical role of the gut-brain axis in neurodegeneration.
内容：
阿尔茨海默病转基因小鼠中，间歇性禁食（IF）减少淀粉样β蛋白（Aβ）积累，诱导海马体基因表达，改善神经炎症。IF作用由肠道微生物来源代谢物吲哚-3-丙酸（IPA）-神经元受体PXR介导。轻度认知障碍和阿尔茨海默病患者的IPA水平低于对照组。IPA补充剂和产IPA胞菌能复制IF的认知益处，而神经元PXR阻断或IPA合成的破坏则使这些益处消失。IPA穿过血脑屏障，展现出强效的抗炎活性，并抑制Aβ的积累，这对神经保护至关重要。这些结果强调了IF调控的微生物代谢产物，尤其是IPA作为AD治疗候选药物，凸显了肠脑轴在神经退行性变性中的关键作用。
2
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标题：
A ubiquitin-like protein controls assembly of a bacterial type VIIb secretion system
一种泛素样蛋白控制细菌VIIb型分泌系统的组装
作者：
Gabriel U Oka, Nathanaël Benoit, Axel Siroy, Francesca Gubellini, Esther Marza, Rémi Fronzes*
链接：
https://pmc.ncbi.nlm.nih.gov/articles/PMC12637312
摘要：
Type VII secretion systems (T7SS) are protein translocation machines crucial for virulence and bacterial competition in Gram-positive bacteria. Despite their importance, the structural basis for assembly of type VIIb secretion systems (T7SSb), a widely distributed variant in Firmicutes, remains poorly understood. We present the cryo–electron microscopy structure of the T7SSb core complex from Bacillus subtilis, revealing how the ubiquitin-like protein YukD, coordinates assembly of the secretion machinery. YukD interacts extensively with the central channel component YukB and facilitates its association with the pseudokinase YukC, forming a stable building block for channel assembly. Time-lapse microscopy and competition assays demonstrate that YukD is essential for proper T7SSb complex formation and contact-dependent bacterial killing. Our findings reveal how bacteria have adapted a ubiquitin-like protein as a structural regulator for assembling a large secretion complex.
内容：
VII型分泌系统（T7SS）对革兰氏阳性菌的毒力和细菌竞争至关重要，但是VIIb型分泌系统（T7SSb）的组装基础仍然了解不充分。本文展示了枯草杆菌T7SSb核心复合体的冷冻电子显微镜结构，揭示了泛素样蛋白YukD与中心通道成分YukB相互作用，促进其与伪激酶YukC的结合，形成通道组装的稳定构建单元。延时显微镜和终点群体竞争检测表明，YukD对于正确形成T7SSb复合物和接触依赖性细菌杀死至关重要。
3
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标题：
Fluidic microgel assemblies with enhanced oral delivery of biologics alleviate colonic inflammation in murine and canine models
增强口服生物制剂的流化微凝胶组件可缓解小鼠和犬类模型中的结肠炎症
作者：
Qingqiao Xie, Chenchen Yan, Zifeng Yang, Xiayi Xu, Yong Li*, Pengchao Zhao*, Liming Bian*
链接：
https://pmc.ncbi.nlm.nih.gov/articles/PMC12694021
摘要：
The efficacy of oral delivery of biologic drugs for inflammatory bowel disease (IBD) treatment is substantially compromised by the swift enzymatic degradation and insufficient retention of biologics in the gastrointestinal tract. Here, we report a simple method for fabricating fluidic microgel assemblies (FMGAs) by introducing the hydrogen bonds between the microgel surfaces. These FMGAs with water content of 77% are flowable yet immiscible with water. Upon oral administration, these FMGAs form a large-area physical adhesive coating on the intestinal surface, extending intestinal retention time to at least 48 hours. The intermicrogel spaces within the assemblies can efficiently harbor therapeutic biologics (such as exosomes and TNFα antibody), protect them from the harsh intestinal microenvironment, and enable efficient delivery to intestinal lesion sites to restore intestinal barrier function and microbiota diversity in mouse and beagle models of IBD. We believe that the fluidic microgel assembly strategy holds great promise for oral delivery of labile biologics for the treatment of diverse gastrointestinal diseases.
内容：
口服生物制剂用于炎症性肠病（IBD）治疗的疗效因消化道内快速的酶降解和生物制剂滞留不足而受限。本文介绍了一种通过引入氢键在微凝胶表面之间制造流体微凝胶组件（FMGA）的简单方法。这些含水量为77%的FMGA可流动且与水不混。口服后，这些FMGAs在肠道表面形成大面积物理粘性涂层，将肠道滞留时间延长至至少48小时。组装体内的微晶间隙能够高效储存治疗性生物制剂（如外泌体和TNFα抗体），保护其免受恶劣肠道微环境的侵害，并高效地输送至肠道病灶部位，以恢复肠屏障功能和微生物多样性，并在小鼠和比格犬IBD模型中得到验证。
4
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标题：
Surface expression of antitoxin on engineered bacteria neutralizes genotoxic colibactin in the gut
在工程细菌表面上表达抗毒素，可以中和肠道内的基因毒素colibactin
作者：
Shaobo Yang, Zongqi Wang, Chengyuan Fang, Mengdi Yang, Saleh Khawaled, Shanna Bonanno, Neel S Joshi, Yun Wei, Ke Zhang, Valeria Márquez-Pellegrin, Ming Guan, Songqi Zhang, Anna Clara Bader, Ningyuan Ye, Amber E Haley, Michael K Dame, Jason R Spence, Xuesong He, James G Fox, Ömer H Yilmaz, Yatrik M Shah, Rizwan Romee, Jiahe Li*
链接：
https://www.nature.com/articles/s41564-025-02177-3
摘要：
Colibactin, a metabolite produced by gut bacteria carrying the polyketide synthase (pks) island, is associated with host genotoxicity and tumorigenesis. However, no Food and Drug Administration-approved therapeutics directly target colibactin. Here we show that expression of the intracellular colibactin self-resistance protein (ClbS) on the surface of engineered bacteria shields the host from genotoxic effects across multiple pks+ isolates. The surface display, due to the fusion of ClbS with outer membrane protein A (ClbS–OmpA) in Escherichia coli, effectively reduced colibactin-induced DNA damage and cell cycle arrest in human cell lines and organoids, outperforming D-serine, a small-molecule inhibitor of colibactin synthesis. The engineered strains mitigated intestinal damage in a mouse model of colitis and suppressed tumorigenesis in mouse models of colon cancer caused by pks+ E. coli. Our results show the feasibility of inhibiting bacterial genotoxins in the gut, establishing a starting point for therapeutics targeting other potential cancer-causing bacterial metabolites.
内容：
Colibactin 是携带聚酮合成酶 (pks) 的肠道细菌产生的代谢产物，与宿主遗传毒性和肿瘤发生有关，没有直接靶向的治疗药物。在这里，作者发现在工程菌表面表达细胞内大肠杆菌Colibactin自身耐药蛋白 (ClbS) 可保护宿主免受多个pks + 分离株的遗传毒性作用。ClbS 与菌外膜蛋白A(ClbS-OmpA) 融合，有效地减少了人细胞系和类器官中大肠杆菌Colibactin诱导的 DNA 损伤和细胞周期停滞，效果优于大肠杆菌Colibactin合成的小分子抑制剂D-丝氨酸。工程菌株减轻了结肠炎小鼠模型中的肠道损伤，并抑制了pks+E. coli引起的结肠癌小鼠模型中的肿瘤发生
5
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标题：
IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity
IL-17介导的抗真菌免疫限制了白念珠菌在口腔中的致病性
作者：
Ricardo Fróis-Martins, Kontxi Martinez de San Vicente, Corinne Maufrais, Sarah Mertens, Natacha Sertour, Emilie Sitterlé, Marie-Elisabeth Bougnoux, Christophe d'Enfert, Salomé LeibundGut-Landmann*
链接：
https://www.nature.com/articles/s41564-025-02198-y
摘要：
Candida albicans is a common resident of the microbiota that supports host homeostasis but can cause disease when immune defences are impaired. Mucocutaneous candidiasis in individuals with IL-17 immune defects provides insights into the immune system's role in controlling C. albicans. Here, using a murine model of oral colonization, we show that IL-17 signalling maintains C. albicans in a non-pathogenic state. Loss of IL-17 leads to fungal filamentation and upregulation of hyphae-associated genes, which is accompanied by epithelial barrier disruption and inflammation, linked to aberrant IL-22 and IL-13 production. The emergence of pathogenic fungal traits was associated with impaired zinc chelation due to reduced calprotectin expression in the IL-17-deficient mice. Prolonged exposure to the immune-dysregulated tissue led to selection of stable, damage-inducing C. albicans variants, mirroring the evolution of isolates from a chronic mucocutaneous candidiasis patient. These findings reveal how IL-17 protects against fungal pathogenicity and how immune dysfunction fosters C. albicans adaptation and diversification within the host.
内容：
白色念珠菌是支持宿主稳态的微生物群中常见的真菌，当免疫防御受损时可能引发疾病。在这里，使用小鼠口腔定植模型，作者发现 IL-17 信号维持白色念珠菌处于非致病状态。IL-17 的缺失导致真菌成丝和菌丝相关基因的上调，伴随上皮屏障破坏和炎症，与异常的 IL-22 和 IL-13 产生有关。在 IL-17 缺陷的小鼠中，由于钙卫蛋白表达减少，致病性真菌性状的出现与锌螯合受损有关。长期暴露于免疫失调组织导致稳定的、损伤诱导的白色念珠菌变体，反映了慢性皮肤粘膜念珠菌病患者分离株的演变。这些发现揭示了 IL-17 如何保护真菌致病性，以及免疫功能障碍如何促进白色念珠菌在宿主内的适应和多样化。
6
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标题：
Gut microbiome-mediated transformation of dietary phytonutrients is associated with health outcomes
肠道微生物介导的膳食植物营养素转化与健康结果相关
作者：
Lu Zhang, Andrea Marfil-Sánchez, Ting-Hao Kuo, Bastian Seelbinder, Loes van Dam, Ana Depetris-Chauvin, Leonie Johanna Jahn, Morten O A Sommer, Michael Zimmermann, Yueqiong Ni*, Gianni Panagiotou*
链接：
https://www.nature.com/articles/s41564-025-02197-z
摘要：
Food, especially plant-based diet, has complex chemical diversity. However, large-scale phytonutrient-metabolizing activities of gut bacteria are largely unknown. Here we integrated and systematically analysed multiple databases containing information on enzymatic reactions and food health benefits, and 3,068 global public human microbiomes. Transformation of 775 phytonutrients from edible plants was associated with enzymes encoded by diverse gut microbes. In vitro assays validated the biotransformation activity of gut species, for example, Eubacterium ramulus. The biotransformation of phytonutrients demonstrated high interpersonal and geographical variability. Machine learning models based on 2,486 public case–control microbiomes, using the abundances of enzymes associated with modification of phytonutrients present in health-associated foods, discriminated the health status of individuals in multiple disease contexts, suggesting altered biotransformation potential in disease. We validated the association of microbiome-encoded enzymes with the anti-inflammatory activity of common edible plants by combining metagenomics and metatranscriptomics analysis in specific-pathogen-free and germ-free mice. These findings have implications for designing precise, personalized diets to guide an individual towards a healthy state.
内容：
食物，尤其是植物性饮食，具有复杂的化学多样性。然而，肠道细菌大规模的植物营养素代谢活性仍大多未知。本研究整合并系统分析了多个包含酶反应和食品健康益处信息的数据库，以及3068个全球公共人类微生物组。从可食用植物转化为775种植物营养素与多种肠道微生物编码的酶相关。体外测验验证了肠道微生物的生物转化活性，例如Eubacterium ramulus 蓝桉真杆菌。植物营养素的生物转化显示出高度的人际和地理差异。本研究通过结合宏基因组学和宏转录组分析，验证了微生物组编码酶与常见食用植物抗炎活性的关联。这些发现对于设计精准、个性化的饮食，引导个体走向健康状态具有重要意义。
7
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标题：
Structure-guided design of a synthetic bile acid that inhibits Clostridioides difficile TcdB toxin
结构引导设计合成胆汁酸，抑制艰难梭菌TcdB毒素
作者：
Sean Miletic, Simoun Icho, Zhijie Li, John Tam, Elizabeth C Rose, Cypress E Perkins, Ali Nakhi, Xinglin Yang, Howard C Hang, John L Rubinstein, Peter I Dosa, Casey M Theriot, Roman A Melnyk*
链接：
https://www.nature.com/articles/s41564-025-02179-1
摘要：
Intestinal bile acids are a family of host and microbiota metabolites that can directly inhibit toxin B (TcdB), the primary virulence factor of Clostridioides difficile that causes infectious diarrhoea and colitis. However, the mechanism underlying the inhibition is unclear. Here we used cryogenic electron microscopy and determined the structure of TcdB bound to inhibitory bile acids cholic acid (methyl ester) and taurochenodeoxycholic acid at 2.9 Å and 3.3 Å resolution, respectively. These structures revealed that bile acids lock the C-terminal CROP domain of TcdB in a conformation that allosterically masks the two receptor-binding sites and prevents target cell recognition. Guided by the structure, we synthesized gut-restricted bile acid derivatives, designed to evade the bile acid reuptake transporters within the gut. One of the derivatives, sBA-2, was retained within the gut upon oral dosing and protected mice from toxin-induced C. difficile disease pathology. Our study uncovers the structural basis of inhibition of TcdB by bile acids and its analogues, paving the way for the development of orally deliverable therapeutics against C. difficile.
内容：
肠道胆汁酸是一类宿主和微生物群代谢产物，能够直接抑制毒素B（TcdB），这是艰难梭菌的主要毒力因子，可导致感染性腹泻和结肠炎。然而，抑制的机制尚不清楚。本研究使用低温电子显微镜，确定了结合于抑制性胆汁酸CA和牛磺鹅去氧胆酸的TcdB结构，表明胆汁酸将TcdB的C端CROP结构域锁定在一种构象中，这种构象在变构方式上掩盖了两个受体结合位点，阻止了目标细胞的识别。在该结构的指导下，本研究合成了胆汁酸衍生物，旨在规避肠道内胆汁酸再摄取转运蛋白，其中一种衍生物sBA-2在口服后被保留在肠道内，保护小鼠免受毒素诱发的艰难梭菌致病。本研究的研究揭示了胆汁酸及其类似物抑制TcdB的结构基础，为口服治疗艰难梭菌的治疗方法的发展铺平了道路。
8
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标题：
Decreased cytoplasmic crowding via inhibition of ribosome biogenesis can trigger Candida albicans filamentous growth
通过抑制核糖体生物合成减少细胞质拥挤可触发白念珠菌丝状生长
作者：
Antonio Serrano, Charles Puerner, Louis Chevalier, Emily Plumb, Johannes Elferich, Stephen Diggs, Ludwig Roman Sinn, Nikolaus Grigorieff, Markus Ralser, Morgan Delarue, Martine Bassilana, Robert Alan Arkowitz*
链接：
https://www.nature.com/articles/s41564-025-02205-2
摘要：
The human fungal pathogen Candida albicans undergoes a morphological transition from a budding yeast to a filamentous form, which is associated with pathogenesis. Various cues mediate this transition including intracellular reorganization. The cytoplasm is densely packed with proteins including large macromolecular complexes, such as ribosomes, and hence, molecular crowding can impact a range of cellular processes. However, the relationship between cytoplasmic molecular crowding and morphological growth states is unclear. Using a fluorescent microrheological probe and single particle tracking, we observed a striking decrease in molecular crowding during filamentous growth in C. albicans. On the basis of simulations, proteomics and structural data from in situ cryogenic electron microscopy, we show that the reduction in crowding is due to a decrease in ribosome concentration that results in part from an inhibition of ribosome biogenesis, combined with an increase in cytoplasmic volume, leading to a dilution of ribosomes. Filamentation was enhanced in a mutant defective in ribosome biogenesis, while translation was not affected, suggesting that inhibition of ribosome biogenesis is a trigger for C. albicans morphogenesis. Overall, we show that filamentous growth is associated with reduced cytoplasmic crowding via changes in ribosome concentration, suggesting that combination therapies in which ribosome biogenesis is also targeted may be advantageous.
内容：
人类真菌病原体白色念珠菌经历从出芽酵母到丝状形态的形态转变，这与发病机制有关。细胞质中富含蛋白质，包括核糖体等大分子复合物，因此分子拥挤会影响一系列细胞过程。然而，细胞质分子拥挤与形态生长状态之间的关系尚不清楚。使用荧光微流变探针和单颗粒追踪，本研究观察到白色念珠菌丝状生长过程中分子拥挤度显著降低。基于模拟、蛋白质组学和原位低温电子显微镜的结构数据，本研究表明拥挤的减少是由于核糖体浓度的降低，部分原因是核糖体生物合成的抑制，再加上细胞质体积的增加，导致核糖体稀释。在核糖体生物合成缺陷的突变体中，丝状化增强，而翻译不受影响，这表明核糖体生物合成的抑制是白色念珠菌形态发生的触发因素。总的来说，本研究发现丝状生长与通过核糖体浓度变化减少细胞质拥挤有关，这表明以核糖体生物合成为靶点的联合疗法可能是有利的。
9
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标题：
Long-read metagenomics for strain tracking after faecal microbiota transplant
粪便微生物群移植后用于株系追踪的长读宏基因组学
作者：
Yu Fan, Mi Ni, Varun Aggarwala, Edward A Mead, Magdalena Ksiezarek, Lei Cao, Michael A Kamm, Thomas J Borody, Sudarshan Paramsothy, Nadeem O Kaakoush, Ari Grinspan, Jeremiah J Faith, Gang Fang*
链接：
https://www.nature.com/articles/s41564-025-02164-8
摘要：
Accurate tracking of bacterial strains that stably engraft in faecal microbiota transplant (FMT) recipients is critical for understanding the determinants of strain engraftment, evaluating correlations with clinical outcomes and guiding the development of therapeutic consortia. While short-read sequencing has advanced FMT research, it faces challenges in strain-level de novo metagenomic assembly. Here we describe LongTrack, a method that uses long-read metagenomic assemblies for FMT strain tracking. LongTrack shows higher precision and specificity than short-read approaches, especially when multiple strains co-exist in the same sample. We uncovered 648 engrafted strains across six FMT cases involving patients with recurrent Clostridioides difficile infection and inflammatory bowel disease. Furthermore, long reads enabled assessment of the genomic and epigenomic stability of engrafted strains at the 5-year follow-up timepoint, revealing structural variations that may be associated with strain adaptation in a new host environment. Our findings support the use of long-read metagenomics to track microbial strains and their adaptations.
内容：
准确追踪能够通过粪便微生物群移植（FMT）稳定植入的细菌株对于理解株系植入决定因素、评估与临床结局的相关性以及指导治疗至关重要。虽然短读序列测序推动了FMT研究，但在宏基因组组装方面面临挑战。本文介绍了LongTrack方法，这是一种利用长读长宏基因组组装进行FMT菌株追踪的方法。LongTrack比短读长方法更为准确、更特异，尤其是在多个菌株共存于同一样本时。本研究在六例FMT病例中发现了648个植入株，患者患有复发性艰难梭菌感染和炎症性肠病。此外，长读长使得5年随访时间点对植入株的基因组和表观基因组稳定性进行了评估，揭示了可能与新宿主环境中菌株适应相关的结构变异。本研究的发现支持使用长读宏基因组学来追踪微生物菌株及其适应性。
10
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标题：
Interkingdom sensing of fungal tyrosol promotes bacterial antifungal T6SS activity in the murine gut
真菌酪醇的跨界感应促进小鼠肠道细菌抗真菌T6SS活性
作者：
Lingfang Zhu, Yuxin Zuo, Rui Cui, Peishuai Fu, Yuqi Liu, Zhuo Wang, Xinquan He, Danyang Yu, Zhiyan Wei, Shuyu Li, Yang Wang, Changfu Li, Yao Wang, De-Feng Li*, Shuang-Jiang Liu*, Xihui Shen*
链接：
https://www.nature.com/articles/s41564-025-02208-z
摘要：
Type VI secretion systems (T6SSs) are molecular machines used by bacteria to release effectors that target either host cells, competing bacteria or fungi. Regulatory mechanisms underlying antifungal T6SS activity remain unexplored. Here we show, using mouse infection with wild-type and T6SS mutant bacteria, that T6SS activity of the enteropathogen, Yersinia pseudotuberculosis (Yptb), reduces fungal prevalence in the gut microbiota and has direct activity on Candida albicans. Screening of bacterial effector mutant strains, and structural and biochemical analyses identify TfeC as an antifungal chitinase T6SS effector that can kill C. albicans. In vivo experiments confirm that TfeC expression promotes Yptb colonization and reduces C. albicans abundance. We also show that Yptb senses the fungal quorum-sensing molecule, tyrosol, through the two-component system, EnvZ–OmpR, and responds by activating T6SS4. Our findings suggest that Yptb modulates its antifungal activities by detecting changes in fungal population density cues, revealing a mechanism of fungal–bacterial interkingdom communication mediated by fungal quorum-sensing molecules.
内容：
VI型分泌系统（T6SSs）是细菌用来释放效应子的分子机器，这些效应子可以攻击宿主细胞、竞争细菌或真菌。抗真菌T6SS活性背后的调控机制尚未被探索。本研究利用野生型和T6SS突变菌感染小鼠，发现伪结核耶尔森氏菌（Yptb）的T6SS活性，可降低肠道微生物群中的真菌感染率，并直接作用于白色念珠菌。通过筛选细菌效应蛋白突变株，以及结构和生化分析，TfeC被识别为一种抗真菌几丁质酶T6SS效应因子，能够杀死白色念珠菌。体内实验证实，TfeC表达促进Yptb定植并减少白念珠菌丰度。本研究还表明Yptb通过EnvZ–OmpR两组分系统感知真菌群体感应分子tyrosol酪醇，并通过激活T6SS4作出反应。本研究的发现表明，Yptb通过检测真菌群体密度的变化来调节其抗真菌活性，揭示了真菌-细菌界间通信的机制，该机制由真菌群体感应分子介导。
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标题：
Anoxia activates CRISPR-Cas immunity in the mouse intestine
缺氧激活小鼠肠道中的CRISPR–Cas免疫
作者：
Ian W Campbell*, David W Basta, Franz G Zingl, Emily J Sullivan, Sudhir Doranga, Matthew K Waldor*
链接：
https://www.nature.com/articles/s41564-025-02172-8
摘要：
The natural context in which CRISPR–Cas systems are active in Enterobacteriaceae has remained enigmatic. Here we find that the Citrobacter rodentium type I-E CRISPR–Cas system is activated by the oxygen-responsive transcriptional regulator Fnr in the anoxic environment of the mouse intestine. Since Fnr-dependent regulation is predicted in ~41% of Enterobacteriaceae cas3 orthologues, we propose that anoxic regulation of CRISPR–Cas immunity is an adaptation that protects Enterobacteriaceae against threats from foreign DNA within the intestinal microbiome.
内容：
自然环境下CRISPR-Cas系统在肠杆菌科中保持活跃仍然是个谜。在这里，作者发现鼠柠檬酸杆菌I-E型CRISPR-Cas系统在小鼠肠道缺氧环境中被氧反应转录调节因子Fnr激活。由于约41%的肠杆菌科cas3直系同源物预测了Fnr依赖性的调节，本研究提出CRISPR-Cas免疫的缺氧调节是一种适应，可以保护肠杆菌科免受肠道微生物组内外源DNA的威胁。
编辑：虞亮
