《科学》（20260212出版）一周论文导读

编译｜冯维维

SCIENCE, 12 FEB 2026，VOLUME 391, ISSUE 6786

《科学》2026年2月12日，第391卷，6786期

Life Science

Structural ontogeny of protein-protein interactions

蛋白质-蛋白质相互作用的结构个体发育

▲ 作者：AERIN YANG, HANLUN JIANG, KEVIN M. JUDE, DENIZ AKPINAROGLU, STEPHAN ALLENSPACH, ALEX JIE LI, JAMES BOWDEN, CARLA PATRICIA PEREZ, LIU LIU, AND K. CHRISTOPHER GARCIA

▲链接：

https://www.science.org/doi/10.1126/science.adx6931

▲摘要：

蛋白质结构研究中的一个长期挑战是理解蛋白质表面如何实现与其他蛋白质的相互作用，最终目标是预测和设计此类表面。然而，科学家仍未完全阐明进化如何塑造这些相互作用。

研究者利用人工蛋白质对的合成共进化方法，探究了蛋白质-蛋白质结合位点的形成与进化机制。

他们发现，在早期阶段形成的初始接触位点，会在结合对共进化过程中呈现多条分化路径。天然界面表面似乎经过预组织，能够快速进化出支持新结合伴侣蛋白相互作用的深层能量阱。

这些见解对于设计合成蛋白质结合物具有重要意义，或可解释抗体和肽类为何常与天然蛋白质结合界面相互作用。

▲ Abstract：

A long-standing challenge in protein structure is understanding how protein surfaces enable interactions with other proteins, with the ultimate goal of predicting and designing such surfaces. However, we still do not fully understand how evolution shapes such interactions. Yang et al. used synthetic coevolution of artificial protein pairs to explore how protein-protein binding sites form and evolve. They identified seed contacts at a very early stage that could take several different paths as the binder pair coevolved. Natural interface surfaces appear to be preorganized to allow fast evolution of deep energy wells that support binding of new partner proteins. These insights will be important to consider when designing synthetic protein binders and may explain why antibodies and peptides often interact with natural protein binding interfaces.

Myelin sheaths in the central nervous system can withstand damage and dynamically remodel

中枢神经系统髓鞘可抵御损伤并动态重塑

▲ 作者：DONIA ARAFA, JULIA VAN DE KORPUT, PHILIPP N. BRAAKER, KIERAN P. HIGGINS, NIELS R. C. MEIJNS, KATY L. H. MARSHALL-PHELPS, JULIA MENG, DANIEL SOONG, ELEONORA SCALIA, AND DAVID A. LYONS

▲链接：

https://www.science.org/doi/10.1126/science.adr4661

▲摘要：

中枢神经系统髓鞘脱失是多种神经系统疾病的标志性特征，但脱髓鞘的具体发生机制尚不明确。研究者利用斑马鱼模型和人体组织研究发现，髓鞘在遭受损伤后、脱落前会经历显著肿胀过程。

斑马鱼活体成像数据显示，髓鞘在某些情况下能够承受广泛损伤并可通过形态重塑实现恢复。

神经元活性的药理调控可影响这种恢复能力，这为预防疾病与衰老过程中的髓鞘丢失提供了潜在治疗策略。

▲ Abstract：

The loss of myelin (demyelination) in the central nervous system is a hallmark of several neurological disorders. However, it remains unclear how the demyelination process occurs. Using zebrafish models and human tissue, Arafa et al. showed that myelin sheets swell drastically after the induction of damage and before being lost. Live imaging data in zebrafish indicated that myelin sheaths can in some cases withstand extensive damage (swelling) and even recover through morphological remodeling. Pharmacological manipulation of neuronal activity can affect this recovery capacity, suggesting a potential therapeutic opportunity to prevent myelin loss in disease and aging.

Mitochondrial control of fuel switching via carnitine biosynthesis

线粒体通过肉碱生物合成调控燃料转换

▲ 作者：CHRISTOPHER AUGER, HIROSHI NISHIDA, BO YUAN, GUILHERME MARTINS SILVA, MASANORI FUJIMOTO, MARK LI, DAISUKE KATOH, DANDAN WANG, MELIA GRANATH-PANELO, AND SHINGO KAJIMURA

▲链接：

https://www.science.org/doi/10.1126/science.ady5532

▲摘要：

人体已进化出根据燃料可用性来利用碳水化合物、脂质或蛋白质供能的适应机制。这种灵活性还有助于通过动用脂肪储备在禁食期间维持生存，同时该机制也参与维持体温的产热过程。这些适应过程依赖于脂肪酸氧化，其中肉碱介导长链脂肪酸向线粒体的转运。

由于膳食摄入的肉碱并不充足（尤其是对于植物性饮食人群），机体必须通过从头合成途径生成肉碱才能维持生存。

研究者阐明了线粒体蛋白SLC25A45在肉碱从头合成中的作用，并在小鼠模型中证实该蛋白对寒冷耐受性及胰高血糖素样肽-1受体激动剂治疗所致体重减轻具有调节效应。

▲ Abstract：

Our bodies have developed adaptations for using carbohydrates, lipids, or proteins as fuels, depending on availability. This flexibility also helps promote survival during fasting by drawing on adipose reserves, and the same mechanism is involved in thermogenesis to maintain body temperature. These adaptations rely on fatty acid oxidation, with carnitine facilitating the transport of long-chain fatty acids into mitochondria. Dietary intake of carnitine is not sufficient, particularly in those who maintain plant-based diets, and thus de novo carnitine synthesis is required for survival. Auger et al. elucidated the role of mitochondrial protein SLC25A45 in de novo carnitine synthesis and demonstrated its effects on both cold tolerance and weight loss on treatment with glucagon-like peptide-1 receptor agonists in mouse models.

Dihydroxyhexanoic acid biosynthesis controls turgor in pathogenic fungi

二羟基己酸的生物合成控制致病真菌的膨压

▲ 作者：NAOYOSHI KUMAKURA, TAKAYUKI MOTOYAMA, KEISUKE MIYAZAWA, TOSHIHIKO NOGAWA, JULIEN PERNIER, KATSUMA YONEHARA, MAYUKO SATO, YUMI GOTO, KAORI SAKAI, AND KEN SHIRASU

▲链接：

https://www.science.org/doi/10.1126/science.aec9443

▲摘要：

多种植物病原真菌通过特化的侵染细胞（附着胞）产生膨压，以机械力突破寄主表皮。

附着胞通过形成半透性细胞壁并积累胞内渗透物质，借助渗透作用产生膨压。尽管已知黑色素对膨压生成至关重要，但细胞壁半透性形成的分子机制尚不明确。

通过反向遗传学手段，研究者发现PKS2与PBG13两种酶是炭疽病菌与稻瘟病菌构建半透性屏障的关键因子。这些酶合成的3,5-二羟基己酸多聚物为真菌致病性所必需，且能在不依赖黑色素的情况下独立降低细胞壁通透性、驱动膨压生成。

研究揭示了真菌膨压生成的新机制，阐明了酶功能与病原菌侵染力之间的关联，为病害防控提供了新靶点。

▲ Abstract：

Many plant pathogenic fungi penetrate host surfaces mechanically, using turgor pressure generated by specialized infection cells called appressoria. These appressoria develop semipermeable cell walls and accumulate osmolytes internally to create turgor by osmosis. Although melanin is known to be important for turgor generation, the mechanism underlying wall semipermeability remains unclear. By using reverse genetics, we identified that the enzymes PKS2 and PBG13 are required for forming the semipermeable barrier in fungi causing anthracnose and rice blast diseases. These enzymes synthesize 3,5-dihydroxyhexanoic acid polymers that are essential for pathogenicity. These polymers reduce cell wall permeability and generate turgor, independently of melanization. Our findings uncover a mechanism of fungal turgor generation, linking enzyme function to pathogen penetration and disease potential, presenting new targets for disease control.

天文学Astronomy

Disappearance of a massive star in the Andromeda Galaxy due to formation of a black hole

仙女座星系中大质量恒星因黑洞形成而消失

▲ 作者：KISHALAY DE, MORGAN MACLEOD, JACOB E. JENCSON, ELIZABETH LOVEGROVE, ANDREA ANTONI, ERIN KARA, MANSI M. KASLIWAL, RYAN M. LAU, ABRAHAM LOEB, AND ROBERT SIMCOE

▲链接：

https://www.science.org/doi/10.1126/science.adt4853

▲摘要：

当一颗大质量恒星到达其生命终点时，其核心坍缩并释放出中微子，这些中微子会驱动一个激波进入恒星外层（包层）。足够强的激波会抛射出包层，从而产生超新星爆发。如果激波未能成功抛射包层，根据理论预测，包层将落回坍缩的核心，形成一个恒星质量的黑洞，并导致该恒星消失。

研究者报告了对M31-2014-DS1的观测，这是一颗位于仙女座星系中、已失去氢包层的超巨星。2014年，它在中红外波段变亮，随后从2017年到2022年，它在光学波段和总光度均变暗了10⁴个数量级（直至无法探测到）。

研究者将这些观测结果，以及先前在NGC 6946星系中观测到的一次事件，解释为形成恒星质量黑洞的失败超新星爆发的证据。

▲ Abstract：

When a massive star reaches the end of its lifetime, its core collapses and releases neutrinos that drive a shock into the outer layers (the stellar envelope). A sufficiently strong shock ejects the envelope, producing a supernova. If the shock fails to eject it, the envelope is predicted to fall back onto the collapsing core, producing a stellar-mass black hole (BH) and causing the star to disappear. We report observations of M31-2014-DS1, a hydrogen-depleted supergiant in the Andromeda Galaxy. In 2014, it brightened in the mid-infrared, then from 2017 to 2022, it faded by factors of10⁴in optical light (becoming undetectable) and in total light. We interpret these observations, and those of a previous event in NGC 6946, as evidence for failed supernovae forming stellar-mass BHs.

生物多样性Biodiversity

Fishing ban halts seven decades of biodiversity decline in the Yangtze River

长江禁渔十年扭转七十年生物多样性衰退

▲ 作者：FANGYUAN XIONG, ZHONGYANG LI, SéBASTIEN BROSSE, JULIAN D. OLDEN, STEVEN J. COOKE, BO YANG, YING LU, WENQI GAO, WEI XIN, AND YUSHUN CHEN

▲链接：

https://www.science.org/doi/10.1126/science.adu5160

▲摘要：

自20世纪50年代以来，中国的快速经济发展引发了前所未有的淡水生物多样性危机。为恢复渔业资源，长江流域自2021年起实施全面禁渔，终止全流域商业捕捞活动。本研究通过评估禁渔前后（2018-2023年）长江干流栖息地的鱼类群落状况，检验这项大规模保护措施的实际成效。

研究发现，持续七十年的生物多样性丧失趋势已得到遏制，鱼类生物量、体型状况、物种多样性均显著提升，受威胁物种开始初步恢复。

除禁渔外，水质改善、水文与河岸生境修复、船舶流量管控等配套措施同样助力生态恢复。这一结果表明，积极的保护行动能够扭转长江生物多样性衰退态势，为全球其他大河流域的生物恢复带来希望。

▲ Abstract：

China’s rapid economic development has triggered an unparalleled freshwater biodiversity crisis since the 1950s. To restore fisheries resources, the Yangtze River Fishing Ban was implemented in 2021 to cease all basin-wide commercial fishing. We evaluate the effectiveness of this large-scale conservation action by assessing fish communities across mainstem habitats before and after the ban (2018 to 2023). The seven-decadal biodiversity loss was halted with improvements in fish biomass, body condition, species diversity, and initial recovery of threatened species. Eliminating fishing pressure was likely key to this recovery, in addition to actions targeting water quality improvement, hydrological and riparian habitat restoration, and vessel traffic reduction. Ambitious conservation actions can halt biodiversity loss in the Yangtze River, bringing hope for biodiversity recovery in other large rivers.