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Photosynthesis under far-red light—evolutionary adaptations and bioengineering of light-harvesting complexes 远红光下的光合作用——光收集复合物的进化适应与生物工程。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-28 DOI: 10.1002/1873-3468.70191
Antonello Amelii, Edoardo Andrea Cutolo, Daniele Montepietra, Claudia Battarra, Roberto Caferri, Stefano Capaldi, Zeno Guardini, Luca Dall'Osto, Roberto Bassi

In plants and algae, photosynthesis is driven by the absorption of sunlight energy by networks of pigments housed within light-harvesting proteins. Special photosynthetic complexes can intercept the low-energy photons corresponding to the far-red spectrum of the photosynthetically active radiation. These so-called red chlorophyll forms are found in multiple lineages of the Viridiplantae clade, are formed upon a change in spatial organization of chromophores within specific subunits of the photosystem I supercomplex, and can be detected by their unique red-shifted fluorescence emission signatures. Red forms enabled phototrophs to colonize light-limited ecological niches, especially where far-red radiation is enriched by leaf shading. The protein environment plays a key role in determining the occurrence of red forms, promoting strong excitonic interactions among chlorophyll a molecules and facilitating their excitation by low-energy photons. In this review, we present a comprehensive account of the evolutionary diversity of long-wavelength-driven photosynthesis in eukaryotes, and detail the biophysical and structural determinants of this phenomenon. Finally, we discuss how this knowledge can be applied in biotechnology to engineer crop canopies with broadened light absorption and higher yield potential.

在植物和藻类中,光合作用是由光收集蛋白质中的色素网络吸收阳光能量驱动的。特殊的光合复合体可以拦截与光合作用有效辐射的远红光谱相对应的低能光子。这些所谓的红色叶绿素形式存在于绿枝植物分支的多个谱系中,它们是在光系统I超复合体的特定亚基内的发色团的空间组织变化中形成的,并且可以通过其独特的红移荧光发射特征来检测。红色形态使光养生物能够在光受限的生态位中定居,特别是在远红色辐射因叶片遮阳而丰富的地方。蛋白质环境在决定红色形态的发生、促进叶绿素a分子之间的强激子相互作用以及促进它们被低能光子激发方面起着关键作用。在这篇综述中,我们全面介绍了真核生物中长波长驱动的光合作用的进化多样性,并详细介绍了这一现象的生物物理和结构决定因素。最后,我们讨论了如何将这些知识应用于生物技术来设计具有更宽光吸收和更高产量潜力的作物冠层。
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引用次数: 0
Targeting EZH2 reverses thyroid cell dedifferentiation and enhances iodide uptake in anaplastic thyroid cancer 靶向EZH2逆转甲状腺细胞去分化并增强间变性甲状腺癌中碘的摄取。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-28 DOI: 10.1002/1873-3468.70207
Diego Claro de Mello, Marcella Maringolo Cristovão, Guilherme Henrique, Vinicius Gonçalves Rodrigues, Caroline Serrano-Nascimento, Edna Teruko Kimura, Cesar Seigi Fuziwara

Anaplastic thyroid carcinoma (ATC) is a highly aggressive malignancy characterized by dedifferentiation and radioiodine refractoriness. We investigated whether EZH2-mediated H3K27me3 deposition represses thyroid differentiation genes (TDGs) in ATC cells. Online ChIP-seq analyses and CUT&RUN confirmed EZH2/H3K27me3 enrichment at key TDGs (SLC5A5, NKX2-1, TSHR, FOXE1, TPO). Pharmacological inhibition of EZH2 with EPZ6438 reactivated TDG expression in RAS and BRAF-mutated ATC cell lines and partially restored iodide uptake. Co-treatment with the MEK1/2 inhibitor U0126 further enhanced TDG expression, consistent with MAPK-dependent regulation of EZH2. These findings reveal EZH2 as a mediator of ATC dedifferentiation and highlight its inhibition as a potential strategy to restore thyroid function and sensitize tumors to radioiodine.

Impact statement

This study reveals how EZH2-driven epigenetic remodeling controls thyroid cell dedifferentiation and loss of iodide uptake in anaplastic thyroid cancer. Our findings provide new mechanistic insights and highlight an FDA-approved drug with repurposing potential, advancing both anaplastic thyroid cancer biology research and therapeutic perspectives.

甲状腺间变性癌(ATC)是一种高度侵袭性的恶性肿瘤,以去分化和放射性碘难治性为特征。我们研究了ezh2介导的H3K27me3沉积是否抑制ATC细胞中的甲状腺分化基因(tdg)。在线ChIP-seq分析和CUT&RUN证实EZH2/H3K27me3在关键tdg (SLC5A5, NKX2-1, TSHR, FOXE1, TPO)富集。在RAS和braf突变的ATC细胞系中,EPZ6438对EZH2的药理学抑制重新激活了TDG的表达,并部分恢复了碘的摄取。与MEK1/2抑制剂U0126共处理进一步增强了TDG的表达,与mapk依赖性EZH2的调控一致。这些发现表明EZH2是ATC去分化的中介,并强调其抑制是恢复甲状腺功能和使肿瘤对放射性碘敏感的潜在策略。本研究揭示了ezh2驱动的表观遗传重塑如何控制间变性甲状腺癌中甲状腺细胞的去分化和碘吸收的丧失。我们的发现提供了新的机制见解,并突出了fda批准的具有重新利用潜力的药物,推进了间变性甲状腺癌的生物学研究和治疗前景。
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引用次数: 0
Phenotypic plasticity including drug efflux drives reversible irinotecan resistance in LIM1215 colorectal cancer cells 包括药物外排在内的表型可塑性驱动LIM1215结直肠癌细胞可逆伊立替康耐药
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-28 DOI: 10.1002/1873-3468.70208
Tugce Dilber, Gizem Damla Yalcin, Kubra Celikbas Yilmaz, Ahmet Acar

Colorectal cancer (CRC) presents significant therapeutic challenges, particularly due to the development of resistance to standard chemotherapeutic agents such as irinotecan. In this study, we aimed to investigate the molecular and phenotypic mechanisms underlying irinotecan resistance in CRC using the LIM1215 cell line model. Transcriptomic analysis demonstrated that drug withdrawal induced major transcriptional reprogramming, characterized by downregulation of ABC transporters (ABCB1 and ABCG2), extracellular matrix-related genes, and markers of epithelial-to-mesenchymal transition (EMT), alongside reactivation of cell cycle pathways. Drug screening further indicated that resistant cells maintained under irinotecan pressure exhibited a multidrug-resistant phenotype, while withdrawn cells regained sensitivity, particularly to tyrosine kinase inhibitors. Supplementation with the efflux inhibitor Elacridar partially restored drug sensitivity in resistant cells, emphasizing the role of transporter-mediated efflux in maintaining resistance.

结直肠癌(CRC)提出了重大的治疗挑战,特别是由于对伊立替康等标准化疗药物的耐药性的发展。在这项研究中,我们旨在利用LIM1215细胞系模型研究CRC中伊立替康耐药的分子和表型机制。转录组学分析表明,药物戒断诱导了主要的转录重编程,其特征是ABC转运蛋白(ABCB1和ABCG2)、细胞外基质相关基因和上皮-间质转化(EMT)标志物的下调,以及细胞周期途径的重新激活。药物筛选进一步表明,在伊立替康压力下维持的耐药细胞表现出多药耐药表型,而退出的细胞恢复了敏感性,特别是对酪氨酸激酶抑制剂。补充外排抑制剂埃拉西达部分恢复了耐药细胞的药物敏感性,强调了转运体介导的外排在维持耐药中的作用。
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引用次数: 0
A Cre-dependent lentiviral vector for neuron subtype-specific expression of large proteins 一个cre依赖的慢病毒载体,用于神经元亚型特异性大蛋白的表达。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-28 DOI: 10.1002/1873-3468.70205
Weixuan Xue, Sandrine Picaud, Régine Hepp, Stéphanie Pons, Uwe Maskos, Bertrand Lambolez, Ludovic Tricoire

Lentiviral vectors are powerful tools for long-term expression of large genes in the mammalian brain, but the palette of lentiviral tools available for targeting specific cell subpopulations is restricted. We describe a lentiviral vector for neuronal subtype-specific expression in Cre mouse lines. Combining a Cre-dependent flip excision switch with a GFP and a 2A self-cleaving peptide, it enables identification of living neurons expressing a gene of interest using fluorescence. We validated this vector by targeting neocortical interneuron types and midbrain dopaminergic neurons. Gene expression occurred exclusively in Cre-expressing neurons without altering their basic electrophysiological properties. This system has been designed to be flexible and easy to modify in order to target expression of any gene of interest in any cell subtype.

慢病毒载体是在哺乳动物大脑中长期表达大基因的强大工具,但用于靶向特定细胞亚群的慢病毒工具的选择是有限的。我们描述了一个慢病毒载体神经元亚型特异性表达在Cre小鼠系。将cre依赖的翻转切除开关与GFP和2A自切割肽相结合,它可以使用荧光识别表达感兴趣基因的活神经元。我们通过针对新皮层中间神经元类型和中脑多巴胺能神经元验证了该载体。基因表达只发生在表达cre的神经元中,而不改变其基本的电生理特性。该系统被设计成灵活且易于修改,以便在任何细胞亚型中靶向表达任何感兴趣的基因。
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引用次数: 0
An intracellular transporter mitigates the CO2-induced decline in iron content in Arabidopsis shoots. 细胞内转运体减轻了二氧化碳引起的拟南芥芽铁含量下降。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-28 DOI: 10.1002/1873-3468.70202
Timothy Mozzanino, Meijie Li, Cécile Fizames, Mattia Adamo, Laurence Lejay, Christian Dubos, Matthieu Platre, Antoine Martin

Rising atmospheric CO2 negatively affects plant iron (Fe) content, yet the underlying mechanisms remain poorly understood. Here, we identified More Iron under elevated CO2 (MIC) as a new player involved in Fe homeostasis under elevated CO2 in Arabidopsis thaliana. MIC is a previously uncharacterized transmembrane protein which we found predominantly localized to the Golgi apparatus. Loss of MIC function results in increased Fe content under elevated CO2, effectively mitigating the Fe decline observed in plants. MIC protein abundance is reduced in roots under elevated CO2, suggesting post-transcriptional regulation of protein stability. This work identifies MIC as a novel component in the plant response to elevated CO2, with potential implications for improving the nutritional quality of crops under climate change.

大气中二氧化碳含量的上升对植物铁(Fe)含量有负面影响,但其潜在机制尚不清楚。本研究发现,拟南芥(Arabidopsis thaliana)在高CO2环境下,更多铁(More Iron under elevated CO2, MIC)在铁稳态中起着新的作用。MIC是一种以前未被发现的跨膜蛋白,我们发现它主要局限于高尔基体。在CO2升高的条件下,MIC功能的丧失导致铁含量的增加,有效地缓解了植物体内铁含量的下降。在二氧化碳浓度升高的情况下,根中MIC蛋白丰度降低,提示了蛋白质稳定性的转录后调控。这项工作确定了MIC是植物对二氧化碳升高响应的一个新成分,对改善气候变化下作物的营养质量具有潜在意义。
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引用次数: 0
Rad27/FEN1 prevents accumulation of Okazaki fragments and ribosomal DNA copy number changes Rad27/FEN1阻止冈崎片段的积累和核糖体DNA拷贝数的改变。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-27 DOI: 10.1002/1873-3468.70193
Tsugumi Yamaji, Yuko Katayama, Nanase Arata, Mariko Sasaki

DNA copy number changes are the most frequent genomic alterations in cancer cells. Here, we demonstrate that Rad27/FEN1, a structure-specific nuclease in budding yeast, plays a crucial role in maintaining the stability of the ribosomal DNA (rDNA) repeats. Severe rDNA instability is observed in the rad27∆ mutant, independently of Fob1-mediated DNA replication fork arrest and DNA double-strand break (DSB) formation in the rDNA. The rad27Δ mutant accumulates Okazaki fragments in the rDNA region, without inducing the formation of detectable DSBs. Similar rDNA instability is observed in DNA ligaseCdc9-deficient cells. Furthermore, Exonuclease 1 and PCNA partially compensate for the loss of Rad27 in rDNA stabilization. These findings highlight the importance of proper Okazaki fragment maturation in the maintenance of rDNA stability.

DNA拷贝数的改变是癌细胞中最常见的基因组改变。在这里,我们证明了出芽酵母中的结构特异性核酸酶Rad27/FEN1在维持核糖体DNA (rDNA)重复序列的稳定性中起着至关重要的作用。在rad27∆突变体中观察到严重的rDNA不稳定,独立于fob1介导的DNA复制叉阻滞和rDNA中DNA双链断裂(DSB)的形成。rad27Δ突变体在rDNA区域积累冈崎片段,而不诱导形成可检测的dsb。在DNA连接酶ecdc9缺陷细胞中也观察到类似的rDNA不稳定性。此外,外切酶1和PCNA部分补偿了rDNA稳定中Rad27的损失。这些发现强调了适当的Okazaki片段成熟在维持rDNA稳定性中的重要性。
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引用次数: 0
Integrative perspectives on signaling, mechanics, and immune interactions in B-cell malignancies b细胞恶性肿瘤的信号、机制和免疫相互作用的综合观点
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-27 DOI: 10.1002/1873-3468.70180
Patricia Pérez-Galán, Martina Seiffert
<p>B-cell malignancies, such as chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL), follicular lymphoma (FL), and diffuse large B-cell lymphoma (DLBCL), represent highly adaptive cancers that persist by exploiting their interactions with the tumor microenvironment (TME) [<span>[1-4]</span>]. Recent advances in molecular biology, single-cell technologies, mechanobiology, and extracellular vesicle (EV) research have provided unprecedented insights into how tumor cells coordinate with stromal and immune components to maintain survival, resist therapy, and evade immune surveillance [<span>[5]</span>]. Collectively, these studies highlight adhesion, intracellular signaling, immune crosstalk, mechanical cues, and vesicle-mediated communication as central processes that define disease progression and therapeutic vulnerabilities. Moreover, several 3D systems have been developed for B-cell neoplasms to better recapitulate disease biology and responses to therapy in a dish [<span>[6]</span>]. This <i>FEBS Letters</i> special issue on “Biology of B-cell malignancies” focuses on recent conceptual and technological advancements that are refining our understanding of the biology of B-cell neoplasms.</p><p>The review article by Laura Gardano, Nadine Varin-Blank, and colleagues describes how adhesion molecules serve as critical regulators connecting cell–cell and cell–matrix interactions with survival pathways, and how their dysregulation promotes protective niches in B-cell malignancies such as CLL and MCL [<span>[7]</span>]. These adhesion-mediated microenvironmental interactions allow malignant cells to withstand stress and resist therapy. Innovative strategies that target adhesion, combined with 3D culture and organ-on-chip models, reveal how mechanical cues further shape cell survival and resistance mechanisms.</p><p>Another related and unexplored topic is the contribution of mechanobiology to B-cell malignancies, here discussed in depth by Sampietro <i>et al</i>. [<span>[8]</span>]. This review article describes how lymphocytes generate, sense, and respond to mechanical stimuli, bridging mechano-transduction, immunology, and cancer cell behavior and response to treatment. The specific measurement methods and bioengineered models are detailed in this review, which also provides an outlook on how manipulation of mechanical cues may improve responses to treatments.</p><p>In this context, B-cell receptor (BCR), integrins, and actin cytoskeleton are fundamental mechano-transducers. In this issue, Pethe and Hartmann review how this network is disrupted in CLL, driving disease progression and therapy resistance. Understanding these mechanisms can improve precision therapies and biomarker-guided treatment strategies [<span>[9]</span>].</p><p>At the intracellular level, the PI3K/AKT pathway governs B-cell proliferation, metabolism, and survival within a tightly balanced “signaling comfort zone,” which is the topic of the review article by Buchner [<span
b细胞恶性肿瘤,如慢性淋巴细胞白血病(CLL)、套细胞淋巴瘤(MCL)、滤泡性淋巴瘤(FL)和弥漫性大b细胞淋巴瘤(DLBCL),是高度适应性的癌症,它们通过利用与肿瘤微环境(TME)的相互作用而持续存在[[1-4]]。分子生物学、单细胞技术、机械生物学和细胞外囊泡(EV)研究的最新进展为肿瘤细胞如何与基质和免疫成分协调以维持生存、抵抗治疗和逃避免疫监视提供了前所未有的见解[[5]]。总的来说,这些研究强调了粘附、细胞内信号、免疫串扰、机械信号和囊泡介导的通讯是定义疾病进展和治疗脆弱性的中心过程。此外,已经为b细胞肿瘤开发了几个3D系统,以更好地概括疾病生物学和对培养皿治疗的反应[b[6]]。这一期《FEBS快报》关于“b细胞恶性肿瘤生物学”的特刊聚焦于最近的概念和技术进步,这些进步正在完善我们对b细胞肿瘤生物学的理解。Laura Gardano, Nadine Varin-Blank及其同事发表的综述文章描述了粘附分子如何作为细胞-细胞和细胞-基质相互作用与生存途径的关键调节因子,以及它们的失调如何促进b细胞恶性肿瘤(如CLL和MCL)中的保护龛[b[7]]。这些粘附介导的微环境相互作用使恶性细胞能够承受压力并抵抗治疗。针对粘附的创新策略,结合3D培养和器官芯片模型,揭示了机械线索如何进一步塑造细胞存活和抵抗机制。另一个相关且未被探索的话题是机械生物学对b细胞恶性肿瘤的贡献,Sampietro等人对此进行了深入讨论[b[8]]。本文综述了淋巴细胞如何产生、感知和响应机械刺激、桥接机械转导、免疫学以及癌细胞的行为和对治疗的反应。本文详细介绍了具体的测量方法和生物工程模型,并展望了操纵机械线索如何改善对治疗的反应。在这种情况下,b细胞受体(BCR)、整合素和肌动蛋白细胞骨架是基本的机械传感器。在这一期中,Pethe和Hartmann回顾了该网络在CLL中如何被破坏,驱动疾病进展和治疗耐药性。了解这些机制可以提高精准治疗和生物标志物引导的治疗策略[b[9]]。在细胞内水平,PI3K/AKT通路在一个紧密平衡的“信号舒适区”内控制b细胞的增殖、代谢和存活,这是Buchner发表的综述文章的主题[[10]]。在CLL中,异常的PI3K/AKT激活驱动疾病进展和治疗耐药,而信号传导过度或不足均可触发细胞死亡。这种双重性强调了选择性破坏白血病细胞中PI3K/AKT信号通路同时保留正常B细胞的治疗潜力。PI3K/AKT也是fox01的主要调节因子,fox01是一种受严格调控的转录因子,根据b细胞分化阶段的不同具有不同的功能。Hlavac等人在这里讨论了它的双重行为和可能的治疗机会[b[11]]。除了内在信号外,肿瘤免疫相互作用强烈影响疾病结局。Llaó-Cid及时回顾了单细胞技术如何绘制b细胞恶性肿瘤中t细胞亚群和功能状态的异质性,揭示了恶性细胞免疫逃避的机制[b[12]]。这些发现不仅完善了我们对T细胞如何在TME中被抑制的理解,而且还提出了在治疗环境中利用或重新激活T细胞反应的策略。结合上述观点,细胞外囊泡(EVs)已成为TME内细胞间通讯的有效介质,Bachurski和Hallek的综述涵盖了这一主题[b[13]]。来自恶性B细胞和免疫细胞的ev运输多种分子货物,包括信号蛋白、检查点分子和代谢物,它们重塑免疫景观并培养耐药性。鉴于它们的异质性和功能复杂性,先进的单ev和单细胞分析平台对于表征ev介导的免疫相互作用和释放它们作为生物标志物和治疗靶点的转化潜力至关重要。最后,在临床前3D模型中,已经投入了大量的努力来概括这种复杂的肿瘤生物学和TME串扰。Faria等人回顾了从2D到3D模型的演变过程,这些模型包含细胞系或患者来源的细胞,包括多种TME线索和细胞类型[[14]]。 作者回顾了不同模型提供的机会和局限性,以概括淋巴瘤生物学和建立临床前治疗平台。总之,这些文章说明了b细胞恶性肿瘤利用微环境线索、细胞内信号传导和免疫调节来确保生存和逃避治疗的多方面策略。粘附分子、PI3K/AKT信号阈值、机械线索、t细胞功能异质性和ev介导的通信作为肿瘤生物学的相互联系层出现,每个层都提供了机制见解和治疗切入点。跨越这些领域的学习告诉我们,成功的治疗策略必须将微环境破坏、机械特性和信号调节与免疫再激活结合起来,而不是孤立地靶向恶性细胞。先进技术的融合,从器官芯片系统到单细胞和单囊泡分析,提供了一个强大的工具箱来剖析这种复杂性,并设计针对b细胞恶性肿瘤动态生态系统的下一代疗法。
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引用次数: 0
The IQ-compete assay for measuring mitochondrial protein import efficiencies in living yeast cells iq竞争测定法用于测定活酵母细胞中线粒体蛋白的输入效率。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-25 DOI: 10.1002/1873-3468.70206
Yasmin Hoffman, Annika Egeler, Saskia Rödl, Johannes M. Herrmann

Most mitochondrial proteins are synthesized in the cytosol and imported into the organelle. Here, we describe a novel Import and de-Quenching Competition (IQ-compete) assay which monitors the import efficiency of model proteins by fluorescence in living cells. For this method, the sequence of the tobacco etch virus (TEV) protease is fused to a mitochondrial precursor and coexpressed with a cytosolic reporter which becomes fluorescent upon TEV cleavage. Thus, inefficient import of the fusion protein leads to a fluorescent signal. With the IQ-compete assay, the import efficiency of proteins can be reliably analyzed in fluorescence readers, by flow cytometry, by microscopy, and by western blotting. We are convinced that the IQ-compete assay will be a powerful strategy for many different applications.

大多数线粒体蛋白在细胞质中合成并输入细胞器。在这里,我们描述了一种新的输入和去猝灭竞争(IQ-compete)实验,该实验通过荧光监测活细胞中模型蛋白的输入效率。在这种方法中,烟草蚀刻病毒(TEV)蛋白酶序列与线粒体前体融合,并与细胞质报告蛋白共表达,该报告蛋白在TEV切割时变成荧光。因此,融合蛋白的无效输入导致荧光信号。使用iq竞争分析,可以通过荧光阅读器、流式细胞术、显微镜和western blotting可靠地分析蛋白质的导入效率。我们相信,智商竞争分析将是一个强大的战略,为许多不同的应用。本文描述了一种监测活酵母细胞中给定蛋白质的线粒体进口效率的新方法。通过这种iq竞争分析,蛋白质进口效率可以通过荧光显微镜、流式细胞术、荧光光谱法或western blotting进行量化。
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引用次数: 0
The anti-CRISPR protein AcrIE8.1 inhibits the type I-E CRISPR-Cas system by directly binding to the Cascade subunit Cas11 抗crispr蛋白AcrIE8.1通过直接结合Cascade亚基Cas11抑制I-E型CRISPR-Cas系统。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-25 DOI: 10.1002/1873-3468.70201
Young Woo Kang, Hyun Ho Park

CRISPR-Cas systems provide adaptive immunity to bacteria by recognizing and destroying foreign genetic elements. The type I-E CRISPR-Cas system utilizes a multi-subunit Cascade complex to detect target DNA and recruit the Cas3 nuclease for degradation. To overcome this defense, bacteriophages have evolved anti-CRISPR (Acr) proteins that inhibit various steps of the CRISPR interference pathway. Here, we determined the crystal structure of AcrIE8.1, an uncharacterized Acr, revealing it binds to Cas11, a Cascade subunit, to disrupt function. AcrIE8.1 has a compact fold with a defined Cas11-binding interface, suggesting a unique inhibitory mechanism among AcrIE proteins. These findings highlight Cas11 as a critical target for Acr-mediated immune evasion.

CRISPR-Cas系统通过识别和破坏外来遗传元素为细菌提供适应性免疫。I-E型CRISPR-Cas系统利用多亚基级联复合体检测目标DNA并招募Cas3核酸酶进行降解。为了克服这种防御,噬菌体进化出抗CRISPR (Acr)蛋白,抑制CRISPR干扰途径的各个步骤。在这里,我们确定了AcrIE8.1(一种未表征的Acr)的晶体结构,揭示了它与Cascade亚基Cas11结合以破坏功能。AcrIE8.1折叠紧凑,具有明确的cas11结合界面,表明其在AcrIE蛋白中具有独特的抑制机制。这些发现强调Cas11是acr介导的免疫逃避的关键靶点。通过结构和生化分析的结合,我们证明了AcrIE8.1直接结合Cascade复合体的Cas11亚基来抑制CRISPR-Cas系统。这代表了一种新的抑制策略,以前没有在AcrIE蛋白中观察到。
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引用次数: 0
It takes a village: preparing women in science for difficult times 这需要一个村庄:让从事科学的女性为困难时期做好准备。
IF 3 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2025-10-23 DOI: 10.1002/1873-3468.70203
Cara Giovanetti

To mark the 10th anniversary of International Day of Women and Girls in Science on 11th February 2025, FEBS Letters opened a writing contest on the topic of female role models in science. We invited entrants not only to reflect on the careers of prominent academics, but also to share stories about the supervisors, colleagues, and other women who have inspired their own research journeys. Here, we present one of two runners-up, an essay by physicist Cara Giovanetti (UC Berkeley and Lawrence Berkeley National Lab), which maps out the challenges faced by women in physical science in an antagonistic political climate through conversations with mentors and colleagues.

为纪念2025年2月11日“妇女和女童参与科学国际日”十周年,FEBS Letters举办了一场以女性科学榜样为主题的写作比赛。我们邀请参赛者不仅要反思杰出学者的职业生涯,还要分享他们的导师、同事和其他女性的故事,这些女性激发了他们自己的研究之旅。在这里,我们展示了两名二等奖中的一名,物理学家卡拉·吉奥瓦内蒂(加州大学伯克利分校和劳伦斯伯克利国家实验室)的一篇文章,通过与导师和同事的对话,描绘了女性在敌对的政治气候下在物理科学领域面临的挑战。
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引用次数: 0
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