Molecular Cell最新文献

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Filament-driven activation of the Kongming antiviral system by deoxyinosine triphosphate 三磷酸脱氧肌苷对孔明抗病毒系统的丝驱动激活

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-02-03 DOI: 10.1016/j.molcel.2026.01.026

Xiangkai Zhen, Yu Li, Zihe Liu, Yang Huang, Xurong Wang, Shuying Xu, Yuchen Jiang, Fan Li, Jinfu Su, Qi Lai, Shaowei Li, Ningshao Xia, Qingbing Zheng, Songying Ouyang

引用次数: 0

Mitochondria as sources and targets of cellular signaling 线粒体作为细胞信号的来源和目标

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-28 DOI: 10.1016/j.molcel.2026.01.008

Anna Meichsner, Verian Bader, Konstanze F. Winklhofer

引用次数: 0

Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus 制造人类核糖体的信号：细胞质和核仁之间的联系

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-28 DOI: 10.1016/j.molcel.2026.01.007

Isabella R. Lawrence, Emily C. Sutton, Shivang Bhaskar, Susan J. Baserga

引用次数: 0

Lysosomes as hubs of metabolic sensing and cellular homeostasis 溶酶体作为代谢传感和细胞稳态的枢纽

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-28 DOI: 10.1016/j.molcel.2026.01.011

Aakriti Jain, Roberto Zoncu

引用次数: 0

Coordinating mRNA maturation: The U1 relay model 协调mRNA成熟：U1中继模型

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-28 DOI: 10.1016/j.molcel.2026.01.006

Yoseop Yoon, Cailyx Quan, Lindsey V. Soles, Yongsheng Shi

mRNA maturation requires precise coordination among transcription, 5′ capping, splicing, and 3′ end formation. Recent biochemical, structural, and genomic studies demonstrate that these processes are tightly coupled through dynamic interactions among RNA polymerase II, the spliceosome, and cleavage–polyadenylation complexes. Here, we synthesize current mechanistic insights into how transcription elongation factors and RNA processing machineries communicate to ensure efficient and accurate transcript maturation. We propose a “U1 relay” model as a unified framework for understanding co-transcriptional splicing and 3′ end formation. We further discuss how RNAs are sorted into nuclear retention/degradation or export pathways based on the RNA processing status. Importantly, RNA processing factors not only act downstream of transcription but also feed back to modulate transcriptional elongation, pausing, and termination, thereby reinforcing bidirectional coupling between RNA synthesis and processing.

mRNA的成熟需要转录、5 ' capping、剪接和3 ' end形成之间的精确协调。最近的生化、结构和基因组研究表明，这些过程通过RNA聚合酶II、剪接体和切割-聚腺苷酸化复合物之间的动态相互作用紧密耦合。在这里，我们综合了目前关于转录延伸因子和RNA加工机制如何沟通以确保有效和准确的转录成熟的机制见解。我们提出了一个“U1中继”模型作为理解共转录剪接和3 '端形成的统一框架。我们进一步讨论了如何根据RNA加工状态将RNA分类为核保留/降解或输出途径。重要的是，RNA加工因子不仅作用于转录的下游，而且还反馈调节转录的延伸、暂停和终止，从而加强RNA合成和加工之间的双向偶联。

引用次数: 0

Mito-nuclear communication: From cellular responses to organismal health 核间通讯：从细胞反应到机体健康

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-28 DOI: 10.1016/j.molcel.2026.01.001

Guanyu Chen, Hangyu Dong, Ye Tian

The co-evolution of mitochondria and the nucleus established constant mito-nuclear communication that is essential for both cellular and organismal homeostasis. At the cell-autonomous level, mitochondrial perturbations activate retrograde pathways such as the mitochondrial unfolded protein response (UPR^mt) and the mitochondrial integrated stress response (ISR^mt), which couple organelle dysfunction to nuclear transcriptional programs, thereby promoting mitochondrial function and preserving cellular integrity. Importantly, this communication is not confined to individual cells but extends across tissues to coordinate systemic adaptations. Stress signals can be sensed, broadcasted through secreted mitokines and neural circuits, and then interpreted by distal organs to coordinate systemic adaptations. These systemic responses integrate metabolism, immunity, and behavior, conferring resilience to stress and shaping the trajectory of aging. Understanding this multi-layered communication, from the organelle to the organism and its microbial ecosystem, promises new therapeutic strategies to enhance mitochondrial function, promote resilience, and extend healthspan.

线粒体和细胞核的共同进化建立了持续的核间通讯，这对细胞和生物体的稳态都是必不可少的。在细胞自主水平上，线粒体扰动激活逆行通路，如线粒体未折叠蛋白反应（UPRmt）和线粒体综合应激反应（ISRmt），它们将细胞器功能障碍与核转录程序结合起来，从而促进线粒体功能并保持细胞完整性。重要的是，这种交流并不局限于单个细胞，而是跨组织扩展以协调系统适应。应激信号可以被感知，通过分泌的分裂因子和神经回路传播，然后由远端器官解释以协调系统适应。这些系统反应整合了代谢、免疫和行为，赋予对压力的弹性，并形成衰老的轨迹。了解这种从细胞器到有机体及其微生物生态系统的多层沟通，有望提供新的治疗策略，以增强线粒体功能，促进恢复力，延长健康寿命。

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引用次数: 0

Why m⁶A? An RNA surveillance model 为什么m⁶?RNA监测模型

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-27 DOI: 10.1016/j.molcel.2026.01.002

D. Dierks, S. Schwartz

N6-methyladenosine (m⁶A) is the most abundant internal modification of mRNA and is most strongly linked to promoting mRNA decay. Why transcripts are born with a death-promoting mark has remained unclear. A previously proposed "fast-track" model posited regulated, gene-specific modulation of m⁶A to coordinate translation and turnover. However, emerging evidence reveals that m⁶A is broadly and mostly constitutively installed at all DRACH motifs except in the vicinity of splice sites, all of which challenge a fast-track model. We propose an "m⁶A surveillance model": properly spliced transcripts mostly evade methylation, while unspliced, transposon-derived, viral, or aberrant RNAs are hypermethylated and selectively degraded. This model reframes m⁶A as a default quality-control mark that flags undesirable unspliced RNAs for removal. We discuss literature supporting and challenging this model as well as experimental priorities that could allow for a more thorough investigation of this model.

n6 -甲基腺苷（m26 A）是mRNA中最丰富的内部修饰，与促进mRNA衰变最密切相关。为什么转录本生来就带有促死标记，目前还不清楚。先前提出的一种“快速通道”模型假设受调控的基因特异性调节26 A来协调翻译和转换。然而，新出现的证据表明，除了剪接位点附近，m 26 A广泛且大部分地安装在所有DRACH基序上，所有这些都挑战了快速通道模型。我们提出了一个“m 26 A监视模型”：正确剪接的转录本大多逃避甲基化，而未剪接的、转座子衍生的、病毒的或异常的rna则被超甲基化和选择性降解。这个模型将m26 A重新定义为默认的质量控制标记，标记不需要的未剪接rna以进行移除。我们讨论了支持和挑战这一模型的文献，以及可以允许对该模型进行更彻底调查的实验优先级。

引用次数: 0

Ribosome-NAC collaboration: A regulatory platform for cotranslational chaperones, enzymes, and targeting factors 核糖体- nac协作：协同翻译伴侣、酶和靶向因子的调控平台

IF 16 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-27 DOI: 10.1016/j.molcel.2025.12.031

Martin Gamerdinger, Nicolas Burg, Elke Deuerling

Protein biogenesis requires the ribosome to collaborate with a diverse set of cotranslational factors that shape the fate of nascent chains. These interactions must be precisely choreographed: while cytonuclear proteins require immediate N-terminal maturation and folding, endoplasmic reticulum (ER) and mitochondrial proteins must be maintained in an unfolded state for targeting to their organelles. Reconciling these opposing demands requires a highly selective sorting mechanism operating at the ribosomal exit tunnel. Recent studies identify the conserved nascent polypeptide-associated complex (NAC) as a central coordinator of this process. By sensing nascent signals and dynamically modulating factor access to the ribosome, NAC directs substrates toward the appropriate maturation or targeting pathway. This emerging framework positions NAC as a molecular hub that organizes cotranslational interactions into efficient and orderly protein-biogenesis pathways. In this review, we discuss the mechanistic principles underlying NAC function and consider broader implications for how ribosome-associated networks enforce fidelity in protein biogenesis.

蛋白质的生物发生需要核糖体与一系列不同的共翻译因子合作，这些共翻译因子塑造了新生链的命运。这些相互作用必须精确编排：当核蛋白需要立即的n端成熟和折叠时，内质网（ER）和线粒体蛋白必须保持在未折叠状态以靶向其细胞器。调和这些对立的需求需要在核糖体出口通道中操作的高度选择性分选机制。最近的研究发现保守的新生多肽相关复合体（NAC）是这一过程的中心协调者。通过感知新生信号和动态调节因子进入核糖体，NAC引导底物走向适当的成熟或靶向途径。这个新出现的框架将NAC定位为一个分子中心，将共翻译相互作用组织成有效和有序的蛋白质生物发生途径。在这篇综述中，我们讨论了NAC功能的机制原理，并考虑了核糖体相关网络如何在蛋白质生物发生中加强保真度的更广泛意义。

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引用次数: 0

RNA anti-CRISPRs deplete Cas proteins to inhibit the CRISPR-Cas system. RNA抗crispr耗尽Cas蛋白抑制CRISPR-Cas系统。

IF 16.6 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-22 Epub Date: 2025-12-30 DOI: 10.1016/j.molcel.2025.12.005

Xiaopan Gao, Kaixiang Zhu, Weihe Zhang, Lin Wang, Linyue Wang, Lei Hua, Tongxin Niu, Bo Qin, Xia Yu, Hongtao Zhu, Sheng Cui

RNA-based anti-CRISPRs (Racrs) interfere with the type I-F CRISPR-Cas system by mimicking the repeats found in CRISPR arrays. Here, we determined the cryo-electron microscopy (cryo-EM) structures of the type I-F crRNA-guided surveillance complex (Csy complex) from Pectobacterium atrosepticum and three RacrIF1-induced aberrant subcomplexes. Additionally, we observed that Cas7f proteins could bind to non-specific nucleic acids, forming right-handed superhelical filaments composed of different Cas7 copies. Mechanistically, RacrIF1 lacks the specific S-conformation observed in the corresponding position of the 5' handle in canonical CRISPR complexes, and it instead adopts a periodic "5 + 1" pattern. This conformation creates severe steric hindrance for Cas5f-Cas8f heterodimer and undermines their binding. Furthermore, Cas7f nonspecifically binds nucleic acids and can form infinite superhelical filaments along Racrs molecules. This oligomerization sequesters Cas6f and Cas7f from binding, therefore blocking the formation of functional CRISPR-Cas effector complexes and ultimately blocking antiviral immunity. Our study provides a structural basis underlying Racrs-mediated CRISPRs inhibition.

基于rna的抗CRISPR （Racrs）通过模仿CRISPR阵列中的重复序列来干扰I-F型CRISPR- cas系统。在这里，我们确定了来自atrosepticum Pectobacterium的I-F型crrna引导的监视复合物（Csy复合物）和三个racrif1诱导的异常亚复合物的冷冻电镜（cro - em）结构。此外，我们观察到Cas7f蛋白可以与非特异性核酸结合，形成由不同Cas7拷贝组成的右旋超螺旋细丝。从机制上讲，RacrIF1缺乏典型CRISPR复合物中5'手柄对应位置观察到的特定s构象，而是采用周期性的“5 + 1”模式。这种构象对Cas5f-Cas8f异源二聚体造成了严重的空间位阻，破坏了它们的结合。此外，Cas7f非特异性结合核酸，可以沿着Racrs分子形成无限的超螺旋细丝。这种寡聚化隔离了Cas6f和Cas7f的结合，从而阻断了功能性CRISPR-Cas效应复合物的形成，最终阻断了抗病毒免疫。我们的研究提供了racrs介导的crispr抑制的结构基础。

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引用次数: 0

IFI16 senses and protects stalled replication forks. IFI16感知并保护停滞的复制分叉。

IF 16.6 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Cell

Pub Date : 2026-01-22 Epub Date: 2026-01-08 DOI: 10.1016/j.molcel.2025.12.024

Amelia Gamble, Thomas A Ward, Otto P G Wheeler, Jessica P Morris, Caryl M Jones, Laura G Bennett, Ellen G Vernon, Vithursha Thanendran, Ilaria Ceppi, Swagata Halder, Damiano Borrello, Thomas D J Walker, Jahnavi Rajan, Hadil Suleiman, Daniel Harrison, Manal Alshetiwi, Gillian Dunphy, Lucy H Jackson-Jones, Petr Cejka, Leonie Unterholzner, Christopher J Staples

Replication stress is a key driver of DNA damage and genome instability. Here, we report that replication stress induces an inflammatory response in the absence of DNA damage. The DNA-sensing factor interferon-γ-inducible factor 16 (IFI16) binds nascent DNA at stalled replication forks and signals via the adaptor stimulator of interferon genes (STING) to induce activation of nuclear factor κB (NF-κB) and the production of pro-inflammatory cytokines, independently of the cytosolic DNA sensor cyclic guanosine monophosphate (GMP)-AMP synthase (cGAS). Replication stress-induced fork remodeling generates a new DNA end that is vulnerable to degradation by nucleases and is protected by a range of factors, including the tumor suppressors BRCA1 and BRCA2. IFI16 acts directly at stalled replication forks to protect nascent DNA from degradation by the nucleases MRE11, EXO1, and DNA2. Furthermore, IFI16 is required for the interferon-mediated rescue of fork protection in BRCA-deficient cells, highlighting the critical role of IFI16 in the crosstalk between innate immunity and fork protection during replication stress.

复制应激是DNA损伤和基因组不稳定的关键驱动因素。在这里，我们报告了复制应激在没有DNA损伤的情况下诱导炎症反应。DNA感应因子干扰素-γ-诱导因子16 （IFI16）通过干扰素基因适配器刺激器（STING）结合停滞复制分叉处的新生DNA，诱导核因子κB （NF-κB）的激活和促炎细胞因子的产生，而不依赖于胞质DNA感应环鸟苷单磷酸(GMP)-AMP合成酶（cGAS）。复制应激诱导的分叉重塑产生一个新的DNA末端，该末端容易被核酸酶降解，并受到一系列因素的保护，包括肿瘤抑制因子BRCA1和BRCA2。IFI16直接作用于停滞的复制叉，以保护新生DNA免受核酸酶MRE11， EXO1和DNA2的降解。此外，在brca缺陷细胞中，IFI16是干扰素介导的叉保护修复所必需的，这突出了IFI16在复制应激过程中先天免疫和叉保护之间的相互作用中的关键作用。

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