《科学》（20260910出版）一周论文导读
《科学》（20260910出版）一周论文导读
编译｜冯维维
Science, 10 SEP 2026,VOLUME 393,ISSUE 6816
《科学》，2026年9月10日，第393卷，6816期
生命科学Life Science
Mechanism of membrane perforation in rotavirus cell entry
轮状病毒进入细胞时膜穿孔的机制
▲ 作者：MARILINA DE SAUTU, CONNY LEISTNER, TOMAS KIRCHHAUSEN, SIMON JENNI, AND STEPHEN C. HARRISON
▲链接：
https://www.science.org/doi/10.1126/science.aeg4851
▲摘要：
无包膜动物病毒的细胞进入需要一个大分子组装体跨细胞膜易位。双链RNA病毒向靶细胞导入一个内部衣壳颗粒，该颗粒不会进一步脱壳。相反，它凭借其内部的聚合酶和加帽活性，将带帽的病毒mRNA挤出。
研究者利用冷冻电子断层扫描技术可视化了恒河猴轮状病毒进入的全过程，从细胞附着、病毒粒子摄取到亚病毒颗粒的释放。
冷冻断层图像以及对分类亚颗粒的亚断层平均，将病毒粒子及其组分的高分辨率结构与活细胞荧光显微镜的时间序列联系起来。研究概述了进入过程中的每一步相应机制，包括将亚病毒颗粒转移至胞质溶胶的膜穿孔步骤。
▲ Abstract：
Cell entry of nonenveloped animal viruses requires translocation of a macromolecular assembly across a cellular membrane. Double-stranded RNA viruses introduce into the target cell an inner capsid particle that does not uncoat further. Instead, it extrudes capped viral mRNA by virtue of polymerase and capping activities within it. As described here, we used cryogenic electron tomography to visualize the full course of rhesus rotavirus entry, from cell attachment and virion uptake to release of the subviral particle. The cryo-tomograms and subtomogram averaging of classified subparticles link high-resolution structures of the virion and its components with time series from live-cell fluorescence microscopy. We outline the mechanism of each step in the entry process, including the membrane perforation step that transfers a subviral particle into the cytosol.
Extensive and differential platinum chemotherapy mutagenesis in livers of children
儿童肝脏中广泛且差异性的铂类化疗致突变作用
▲ 作者：ANNA WENGER, JEAN-BAPTISTE VANNIER, HENRY LEE-SIX, ROBIN LOESCH, GIULIA EMANUELLI, MANAS DAVE, MEHDI LAYEGHIFARD, ANDREW R. J. LAWSON, FEDERICO ABASCAL, AND SAM BEHJATI, etc.
▲链接：
https://www.science.org/doi/10.1126/science.ady0339
▲摘要：
儿童癌症如今比以往任何时候都更可治疗，但这些治疗本身也带来风险。儿童癌症幸存者可能经历多种长期健康后果，其中一些尚未被完全理解。
人们普遍知道，化疗等癌症治疗会在多种健康组织中引起突变，研究者鉴定出一种由治疗引起的组织特异性致突变模式。其研究证明，铂类药剂——其中最引人注目的是顺铂，是儿童癌症治疗方案中的常见组成部分，会在肝脏中特异性地诱导一种特定的突变特征，这可能解释了某些后期不良反应。
▲ Abstract：
Pediatric cancers are now more treatable than they have ever been before, but the treatments come with their own risks. Survivors of pediatric cancer can experience multiple long-term health consequences, some of which are not fully understood. It is generally known that cancer treatments such as chemotherapy cause mutations in a variety of healthy tissues, but Wenger et al. identified a tissue-specific mutagenic pattern resulting from treatment (see the Perspective by Vasudevan and Parsons). The authors demonstrated that platinum-based agents, most notably cisplatin, which is a common part of pediatric cancer treatment regimens, induce a particular mutational signature specifically in the liver, potentially explaining some of the later adverse effects.
Unphosphorylated tyrosines mediate PD-1 inhibition of T cell signaling condensate formation
未磷酸化酪氨酸介导 PD-1对T细胞信号凝聚体形成的抑制
▲ 作者：MONICA SHARMA, ZACHARY B. KATZ, DAVID C. DEWITT, KIERSTEN M. RUFF, AKASHDIP SINGH, HUAN LAN, WILSON PHUNG, JEFFERY TOM, AIMIN SONG, AND ANDREY S. SHAW
▲链接：
https://www.science.org/doi/10.1126/science.adt9365
▲摘要：
T细胞受体（TCR）结合抗原后，会诱导形成包含支架蛋白活化T细胞连接蛋白（LAT）的生物分子凝聚体。研究探讨免疫抑制性受体程序性细胞死亡蛋白 1（PD-1）是否通过阻碍TCR诱导的LAT凝聚来发挥抑制作用。
体外重组实验表明，PD-1胞内结构域可直接抑制LAT凝聚；该抑制性相互作用依赖PD-1两个抑制基序中的酪氨酸残基。与现有主流模型相反，酪氨酸磷酸化会消除PD-1的这种抑制效应。
将酪氨酸突变为色氨酸可在T细胞中重建PD-1的抑制功能，证实磷酸化并非介导该抑制作用的机制。该结果支持如下理论：抑制基序内能够提供氢键的芳香族残基，是抑制性受体扰乱信号网络、阻断免疫活化的核心作用机制。
▲ Abstract：
T cell receptor (TCR) engagement stimulates formation of a biomolecular condensate, including the scaffold protein linker of activated T cells (LAT). We investigated whether the immune-inhibitory receptor programmed cell death protein 1 (PD-1) inhibits by impeding TCR-induced LAT condensation. In vitro reconstitutions revealed that the cytoplasmic domain of PD-1 directly inhibited LAT condensation. This inhibitory interaction required tyrosine residues in the two inhibitory motifs of PD-1. Contrary to current working models, tyrosine phosphorylation eliminated PD-1 inhibition. Replacing tyrosine with tryptophan reconstituted PD-1 inhibition in T cells, confirming that phosphorylation does not mediate this effect. These findings support the concept that hydrogen bond–donating aromatic residues within inhibitory motifs provide the primary mechanism that explains how inhibitory receptors disrupt signaling networks and block immune activation.
物理学Physics
Discovery of an intrinsic non-Hermitian phase transition in a bulk condensed-matter system
发现体态凝聚态系统中的内禀非厄米相变
▲ 作者：JINGWEN LI, MICHAEL TURAEV, MASAKAZU MATSUBARA, KRISTIN KLIEMT, CORNELIUS KRELLNER, SHOVON PAL, MANFRED FIEBIG, AND JOHANN KROHA
▲链接：
https://www.science.org/doi/10.1126/science.ady4670
▲摘要：
在常规相变中，系统保持热平衡。然而，当系统被驱动至远离平衡态时，可能会出现非厄米相变，其中发生定性变化的是动力学行为——而非稳态性质——并且发生在被称为奇异点的临界点处。研究者通过实验在体态凝聚态系统中实现了非厄米相变。
光激发在铁磁氧化铕中产生电荷载流子。在与向铁磁有序的厄米相变之间的温度依赖相互作用中，弛豫动力学发生了非厄米变化，并在时间分辨反射数据中表现为从双指数实数衰减到单指数复数衰减的转变。
该理论对这一行为进行了建模，表明非厄米相变可能在体态凝聚态物质中普遍出现。
▲ Abstract：
Across regular phase transitions, systems remain in thermal equilibrium. However, when a system is driven far from equilibrium, non-Hermitian phase transitions may arise where the dynamical behavior—rather than steady properties—undergoes a qualitative change at a critical, so-called exceptional point. We experimentally realize a non-Hermitian phase transition in a bulk condensed-matter system. Optical excitation creates charge carriers in ferromagnetic europium monoxide. In a temperature-dependent interplay with the Hermitian transition to ferromagnetic order, a non-Hermitian change of the relaxation dynamics occurs, manifesting in our time-resolved reflection data as the transition from biexponential real to single-exponential complex decay. Our theory models this behavior and suggests that non-Hermitian phase transitions may generically emerge in bulk condensed matter.
Giant tunneling electroresistance in sliding ferroelectrics
滑动铁电体中的巨隧穿电致电阻
▲ 作者：Giant tunneling electroresistance in sliding ferroelectrics
▲链接：
https://www.science.org/doi/10.1126/science.aeh3697
▲摘要：
非易失性存储器应能在消耗极少能量的同时可靠地存储信息。铁电隧道结提供了紧凑的读出方式，但传统的离子位移铁电体会疲劳，而二维滑动铁电体虽然稳健，却在两端器件中产生较弱的读出信号。
研究者设计了一种范德华结，使用菱方相二硫化钼、六方氮化硼、单层石墨烯和铬。该架构将微小的滑动极化转化为对隧穿势垒高度和载流子浓度的协同调制。
这些器件表现出超过1000万的隧穿电致电阻，在0.5伏下高电导态电流密度为222安培每平方厘米，耐久性超过1000亿次循环，同时以13纳秒脉冲进行开关，估算能量为6.5飞焦，为紧凑型低功耗存储器提供了一条途径。
▲ Abstract：
Nonvolatile memories should store information reliably while consuming little energy. Ferroelectric tunnel junctions offer compact readout, but conventional ionic displacement ferroelectrics can fatigue, and two-dimensional sliding ferroelectrics are robust but generate weak readout in two terminal devices. We engineered a van der Waals junction using rhombohedral molybdenum disulfide, hexagonal boron nitride, monolayer graphene, and chromium. This architecture converts small sliding polarization into synergistic modulation of tunneling barrier height and carrier concentration. The devices showed tunneling electroresistance above 10 million, a high conductance state current density of 222 amperes per square centimeter at 0.5 volts, and an endurance beyond 100 billion cycles while switching with 13-nanosecond pulses at an estimated energy of 6.5 femtojoules, offering a route to compact low-power memory.
Endurance beyond 10 billion cycles in wurtzite ferroelectrics by confining nitrogen vacancies
通过限制氮空位实现纤锌矿铁电体超过100亿次循环的耐久性
▲ 作者：RUIQING WANG, FENG ZHU, HAOJI QIAN, JIUREN ZHOU, WENXIN SUN, SIYING ZHENG, JIAJIA CHEN, BOCHANG LI, YAN LIU , AND GENQUAN HAN
▲链接：
https://www.science.org/doi/10.1126/science.aec7337
▲摘要：
纤锌矿铁电体可为晶圆级集成铁电存储器提供一条途径，但受限于耐久性，通常在大约10?次循环时失效。研究者确定氮空位（VN）聚集和长程渗流迁移是驱动漏电流增长和介电击穿的缺陷介导路径。
他们将空间工程化的氮化铝钪/氮化铝（AlScN/AlN）超晶格与动态恢复方案相结合，以在空间和能量上限制VN演化，从而在循环电应力下稳定缺陷拓扑，并抑制硬击穿和铁电退化。并在完全翻转标准（剩余极化≥ 100微库仑每平方厘米）下，展示了纤锌矿铁电体超过101?次循环的耐久性。
这些发现确立了VN限制作为一种可扩展的缺陷拓扑框架，将原子尺度缺陷稳定性与可靠的超密集铁电存储器联系起来，并为下一代非易失性存储器技术提供了指导。
▲ Abstract：
Wurtzite ferroelectrics could provide a route to wafer-scale integrated ferroelectric memories but are limited by endurance, typically failing at ~10? cycles. We identified nitrogen-vacancy (VN) clustering and long-range percolative migration as the defect-mediated pathways that drive leakage-current growth and dielectric breakdown. We combined a spatially engineered aluminum scandium nitride/aluminum nitride (AlScN/AlN) superlattice with a dynamic recovery protocol to spatially and energetically confine VN evolution that stabilized defect topology under cyclic electrical stress and suppressed hard breakdown and ferroelectric degradation. We demonstrated endurance beyond 1010 cycles in wurtzite ferroelectrics under a complete-switching criterion (remnant polarization ≥ 100 microcoulombs per square centimeter). These findings establish VN confinement as a scalable defect-topology framework that couples atomic-scale defect stability to reliable ultradense ferroelectric memories and provide guidance for next-generation nonvolatile memory technologies.