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Loss and gain of motor protein function cause microtubule bundle damage in Drosophila axons. 运动蛋白功能的丧失和获得引起果蝇轴突微管束损伤。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-19 DOI: 10.1016/j.cub.2025.12.038
Yu-Ting Liew, Milli Owens, David M D Bailey, William Cairns, Maureece Day, Ella Jones, Sophie McCann, Lydia Lorenzo-Cisneros, Thomas Murphy, Jill Parkin, Haydn Tortoishell, Federico Dajas-Bailador, Matthias Landgraf, Devesh C Pant, André Voelzmann, Andreas Prokop

Neurodegeneration often starts by atrophy of the cable-like nerve fibers (axons) that wire nervous systems. Maintaining axons requires supply via motor-protein-driven transport along uninterrupted bundles of microtubules. Functional loss of motor proteins, but surprisingly also their hyperactivation, links to conditions of axonal atrophy; in both cases the underlying mechanisms are little understood. To bridge this important knowledge gap, we carried out systematic studies using 40 different genetic tools to manipulate 19 context-related genes in one standardized Drosophila primary neuron system. Starting with transport motors, we found that downregulation in at least three of them-dynein heavy chain, the kinesin family member 5 (KIF5) ortholog kinesin heavy chain (Khc), and KIF1A ortholog Unc-104-caused disintegration of axonal microtubule bundles, which we refer to as "microtubule-curling"; this damages the essential highways for life-sustaining axonal transport. To understand this phenomenon, we focused on Khc's various subfunctions. We found that abolishing Khc-mediated mitochondrial and lysosomal transport affects the homeostasis of reactive oxygen species (ROS), which in turn triggers microtubule-curling in fly and mouse neurons alike. Taking the opposite approach by using conditions where Khc is hyperactive, we observed comparable microtubule-curling, triggered by an ROS-independent mechanism likely involving excessive mechanical force generation. To assess wider relevance of our findings, we studied Unc-104, its binding partner KIF-binding protein (KIFBP), and human KIF5A. These studies suggest that functional loss and hyperactivation of other transport motors also cause ROS-dependent and -independent microtubule-curling, which could therefore represent two fundamental pathways that link transport motors to microtubule bundle decay and neurodegeneration.

神经变性通常始于连接神经系统的索状神经纤维(轴突)的萎缩。维持轴突需要通过马达蛋白驱动的沿着不间断微管束的运输来供应。运动蛋白的功能丧失,但令人惊讶的是它们的过度激活,与轴突萎缩有关;在这两种情况下,人们对其潜在机制知之甚少。为了弥补这一重要的知识差距,我们进行了系统的研究,使用40种不同的遗传工具来操纵一个标准化的果蝇初级神经元系统中的19个上下文相关基因。从运输马达开始,我们发现其中至少三个-动力蛋白重链,激酶家族成员5 (KIF5)同源激酶重链(Khc)和KIF1A同源unc -104的下调导致轴突微管束解体,我们称之为“微管卷曲”;这破坏了维持生命的轴突运输的重要通道。为了理解这种现象,我们将重点放在Khc的各个子函数上。我们发现,取消khc介导的线粒体和溶酶体运输会影响活性氧(ROS)的稳态,从而引发果蝇和小鼠神经元中的微管卷曲。采用相反的方法,在Khc过度活跃的条件下,我们观察到类似的微管卷曲,由ros独立机制触发,可能涉及过度的机械力产生。为了评估我们的发现的更广泛的相关性,我们研究了Unc-104,它的结合伙伴KIFBP (KIFBP)和人类KIF5A。这些研究表明,其他运输马达的功能丧失和过度激活也会导致ros依赖性和非依赖性微管卷曲,因此,这可能代表了将运输马达与微管束衰变和神经变性联系起来的两条基本途径。
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引用次数: 0
Posterior parietal cortex maps progress along routes sharing the same meta-structure but opposite action series. 后顶叶皮层沿着共享相同元结构但相反的动作系列的路线绘制进展图。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-22 DOI: 10.1016/j.cub.2025.12.042
Alexander B Johnson, Emily Xu, Douglas A Nitz

Path networks defined by patterns of intersections and orientations among individual paths may contain recurrent meta-structural features that can be learned and used in spatial reasoning and navigation.1 Posterior parietal cortex (PPC) neurons exhibit scalable tuning to progress through routes,2 suggesting that PPC in rats, as in humans, may function to encode common structure among multiple routes.3,4,5,6 PPC neurons were recorded as rats performed a spatial working memory task within a network organized by recurrence in the layout of short and long pathways and right angle intersections. The specific routes utilized provided opportunity to contrast responses of PPC sub-populations to navigational actions with more complex responses that map route progress and features of route structure. We found evidence for the presence of PPC neurons that generalize in their firing patterns across routes having the same shape but opposite action series. A separate population discriminated the same routes and exhibited activity more closely related to angular velocity. The results indicate that PPC has the capacity to generalize the mapping of route progress and meta-structural organization in parallel with encoding of navigational actions. We suggest that such encoding can form the basis for learning the meta-structural organization of a non-random path network structure, such as that commonly found in cities. Further, the findings suggest that PPC could compute relationships between higher-order spatial information and navigational action sequences.

由个体路径之间的交叉和方向模式定义的路径网络可能包含可在空间推理和导航中学习和使用的反复元结构特征后顶叶皮层(PPC)神经元表现出可扩展的调节机制,2表明大鼠的PPC和人类一样,可能在多种通路中编码共同结构当大鼠执行空间工作记忆任务时,PPC神经元被记录在一个由长、短通路和直角交叉点布局的递归网络中。所使用的特定路线提供了将PPC亚种群对导航行为的反应与更复杂的反应(映射路线进展和路线结构特征)进行对比的机会。我们发现了PPC神经元存在的证据,这些神经元在具有相同形状但相反的动作系列的路线上泛化其放电模式。一个单独的种群区分相同的路线,并表现出与角速度更密切相关的活动。结果表明,PPC在对导航行为进行编码的同时,具有对路径进程映射和元结构组织进行概括的能力。我们认为这种编码可以形成学习非随机路径网络结构的元结构组织的基础,例如在城市中常见的网络结构。此外,研究结果表明,PPC可以计算高阶空间信息和导航动作序列之间的关系。
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引用次数: 0
Bacterial competition: How to hotwire a flagellum. 细菌竞争:如何使鞭毛发热。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 DOI: 10.1016/j.cub.2025.12.015
Geoffrey B Severin, Christopher M Waters

Translocation of an effector from one soil microbe into a competitor forces the recipient to swim away using a mechanism that bypasses canonical cyclic di-GMP repression of flagellar gene biosynthesis.

将一种效应物从一种土壤微生物转移到另一种竞争微生物中,利用一种绕过鞭毛基因生物合成的典型环二gmp抑制的机制,迫使接受者游走。
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引用次数: 0
Evolution: In the monkey mating game, misinformation saves lives. 进化:在猴子的交配游戏中,错误的信息可以拯救生命。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 DOI: 10.1016/j.cub.2025.12.043
Melissa Emery Thompson

During transitions to a new leader male, gelada infants face a serious risk of infanticide. New research demonstrates that mothers reduce this risk by misrepresenting their fertility status.

在向新的雄性领袖过渡的过程中,狒狒幼崽面临着严重的杀婴风险。新的研究表明,母亲通过谎报自己的生育状况来降低这种风险。
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引用次数: 0
Soma Ca2+ is decoupled from daily synaptic activity and neuropeptide release in Drosophila clock neurons. 在果蝇时钟神经元中,体细胞Ca2+与日常突触活动和神经肽释放脱钩。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-12 DOI: 10.1016/j.cub.2025.12.010
Markus K Klose, Junghun Kim, Sydney N Gregg, Brigitte F Schmidt, Xiju Xia, Yulong Li, Edwin S Levitan

Drosophila sLNv clock neurons release the co-packaged neuropeptides PDF and sNPF to regulate circadian behaviors and nighttime sleep.1,2,3,4 Many studies of membrane potential and cytoplasmic Ca2+ at the sLNv soma emphasized elevations late at night or in the very early morning,5,6,7,8,9 although action potential activity and synaptic release were not quantified. Recently, exocytosis of neuropeptide-containing dense-core vesicles (DCVs) at sLNv terminals was found to peak hours later at midmorning.10 To resolve the basis of the timing mismatch between somatic measurements and terminal exocytosis, recently developed probes were used to measure daily rhythms in sLNv neuron synaptic Ca2+ and sNPF release. Remarkably, at midmorning after soma Ca2+ has dropped, both Ca2+ spiking and clock-dependent native neuropeptide release peak in the distal terminals of the protocerebrum. Furthermore, Ca2+ in the soma and terminals differ in dependence on Ca2+ influx. Finally, synaptic DCV exocytosis requires Ca2+ spike activity at terminals that is not evident at the soma. These results lead to two striking conclusions. First, soma Ca2+ recording, which is the focus of many circuit studies, is not indicative of presynaptic Ca2+ and neuropeptide release in distal sLNv terminals. Second, daily clock- and activity-dependent sLNv terminal neuropeptide release occurs many hours in advance of known sLNv neuropeptide effects on nighttime sleep and morning behavior.

果蝇sLNv时钟神经元释放共包装神经肽PDF和sNPF来调节昼夜行为和夜间睡眠1,2,3,4许多关于sLNv胞体膜电位和细胞质Ca2+的研究强调了深夜或清晨的升高,5,6,7,8,9,尽管动作电位活性和突触释放未被量化。最近,在sLNv末端发现含有神经肽的致密核囊泡(DCVs)的胞外分泌在上午10点后达到高峰为了解决体细胞测量和终端胞外分泌之间的时间不匹配的基础,最近开发的探针被用来测量sLNv神经元突触Ca2+和sNPF释放的日常节律。值得注意的是,在上午上午,在体细胞Ca2+下降后,Ca2+峰值和时钟依赖性天然神经肽释放在原大脑远端达到峰值。此外,Ca2+在胞体和终末对Ca2+内流的依赖性不同。最后,突触DCV胞外分泌需要Ca2+尖峰活性在末端,这是不明显的在体细胞。这些结果引出了两个惊人的结论。首先,胞体Ca2+记录,这是许多电路研究的重点,并不表明突触前Ca2+和神经肽在远端sLNv终端释放。其次,每天的生物钟和活动依赖于sLNv末端神经肽的释放,比已知的sLNv神经肽对夜间睡眠和早晨行为的影响提前了许多小时。
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引用次数: 0
Soybean maintained immunodiversity during domestication despite a significant loss in genetic diversity. 大豆在驯化过程中保持了免疫多样性,尽管遗传多样性显著丧失。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-09 DOI: 10.1016/j.cub.2025.11.070
Yan Lai, Bradley Laflamme, Nadia Morales, Clare Breit-McNally, Tamar V Av-Shalom, Pauline W Wang, Albert U Tenuta, Francois Belzile, Darrell Desveaux, David S Guttman

Soybean (Glycine max (L.) Merr.) is one of the most economically important crops in the world, but every year, pathogens cause billions of dollars' worth of losses worldwide. The domestication of this critical crop was associated with several severe genetic bottlenecks that resulted in a dramatic loss of genetic diversity (∼50%) relative to its wild progenitor. Although domestication selected for favorable agricultural traits, it is unclear how the reduced genetic diversity affected the immunity landscape of cultivated soybean relative to its wild ancestors. We performed a comprehensive screen for effector-triggered immune (ETI) responses of both cultivated soybean (Glycine max) and wild soybean (Glycine soja) against the bacterial speck pathogen Pseudomonas syringae. We uncovered an extensive ETI landscape in both species, with 121/529 alleles (22.9%) from 32/65 effector families (49.2%) eliciting ETI in G. max and 125/529 alleles (23.6%) from 23/65 effector families (35.4%) eliciting ETI in G. soja. Interestingly, soybean recognized all three effectors encoded in the conserved effector locus (CEL) of P. syringae (AvrE, HopM, and HopAA), providing pervasive and stacked resistance against this common soybean pathogen. Finally, we demonstrate that pretreatment of soybean with the CEL effectors can immunize soybean against subsequent infection. Overall, we have defined the ETI landscape of soybean against P. syringae and demonstrated that domestication has not compromised soybean immunodiversity despite a dramatic loss in genetic diversity.

大豆(甘氨酸max (l))小麦是世界上最重要的经济作物之一,但每年,病原体在世界范围内造成数十亿美元的损失。这种重要作物的驯化与几个严重的遗传瓶颈有关,导致与其野生祖先相比遗传多样性急剧下降(约50%)。虽然驯化选择了有利的农业性状,但目前尚不清楚遗传多样性的减少如何影响栽培大豆相对于其野生祖先的免疫景观。我们对栽培大豆(Glycine max)和野生大豆(Glycine soja)对细菌斑点病原体丁香假单胞菌的效应触发免疫(ETI)反应进行了全面筛选。结果表明,在大豆和黄豆中,分别有来自32/65效应家族的121/529等位基因(22.9%)和来自23/65效应家族的125/529等位基因(23.6%)和来自32/65效应家族的35.4%的等位基因(23.6%)在黄豆和黄豆中引发ETI。有趣的是,大豆识别了丁香假单胞菌保守效应位点(CEL)中编码的所有三种效应因子(AvrE, HopM和HopAA),提供了对这种常见大豆病原体的普遍和累积抗性。最后,我们证明了用CEL效应物预处理大豆可以使大豆免疫抵抗后续侵染。总的来说,我们已经定义了大豆对丁香假单胞菌的ETI景观,并证明驯化并没有损害大豆的免疫多样性,尽管遗传多样性急剧下降。
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引用次数: 0
Mechanical force locally damages, remodels, and stabilizes the lattice of spindle microtubules. 机械力局部破坏、重塑和稳定纺锤微管晶格。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-23 DOI: 10.1016/j.cub.2025.12.047
Caleb J Rux, Megan K Chong, Valerie Myers, Nathan H Cho, Sophie Dumont

To segregate chromosomes at cell division, the spindle must maintain its structure under force. How it does so remains poorly understood. To address this question, we use microneedle manipulation to apply local force to spindle microtubule bundles, kinetochore fibers (k-fibers), inside mammalian cells. We show that local load directly fractures k-fibers and that newly created plus-ends often have arrested dynamics, resisting depolymerization. Force alone, without fracture, is sufficient for spindle microtubule stabilization, as revealed by laser ablating k-fibers under local needle force. Doublecortin, which binds a compacted microtubule lattice, is lost around the force application site, suggesting local force-induced structural remodeling. In turn, end-binding protein 1 (EB1), which recognizes guanosine triphosphate (GTP)-tubulin, is locally enriched at stabilization sites, both before and after force-induced fracture. Together, our findings support a model in which force-induced damage leads to local spindle microtubule lattice remodeling and stabilization, which we propose reinforces the spindle where it experiences critical loads.

为了在细胞分裂时分离染色体,纺锤体必须在外力作用下保持其结构。人们对它是如何做到的仍知之甚少。为了解决这个问题,我们使用微针操作对哺乳动物细胞内的纺锤体微管束,着丝点纤维(k-纤维)施加局部力。我们发现局部载荷直接使k-纤维断裂,并且新产生的正端通常具有抑制动力学,抵抗解聚。激光烧蚀k-纤维在局部针力作用下的实验结果表明,单靠力而非断裂足以稳定纺锤体微管。结合紧致微管晶格的双皮质素在受力部位周围丢失,提示局部受力引起的结构重塑。反过来,识别鸟苷三磷酸(GTP)-微管蛋白的末端结合蛋白1 (EB1)在力致骨折前后的稳定位点都局部富集。总之,我们的研究结果支持了一个模型,在这个模型中,力诱导的损伤导致了局部纺锤微管晶格的重塑和稳定,我们认为这加强了纺锤在经受临界载荷的地方。
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引用次数: 0
Motivation under aversive conditions is regulated by a striatopallidal pathway in primates. 灵长类动物在厌恶条件下的动机是由纹状体通路调节的。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-09 DOI: 10.1016/j.cub.2025.12.035
Jung-Min N Oh, Satoko Amemori, Ken-Ichi Inoue, Kei Kimura, Masahiko Takada, Ken-Ichi Amemori

Motivation often diminishes under aversive conditions. Clinically, motivational deficits are linked to psychiatric disorders such as depression and schizophrenia, yet the neural mechanisms by which aversive contexts suppress motivation remain unclear. Although classical theories associate motivation with the expected value of outcomes, less is known about the neural circuits that govern effort-based behavioral initiation. To address this, we dissociated motivational drive from goal valuation using an approach-avoidance (Ap-Av) task, in which macaques evaluated outcomes combining reward and punishment (air puffs to the face). As a control, we employed an approach-approach (Ap-Ap) task based solely on reward. Using chemogenetic manipulation, we found that selective inhibition of the ventral striatum to ventral pallidum (VS-VP) pathway restored the motivation to initiate trials in the Ap-Av task without affecting goal valuation. No effects were observed in the Ap-Ap task. These findings provide causal evidence that the VS-VP pathway mediates motivational suppression in aversive contexts. Electrophysiological recordings revealed rapid VS responses to aversive cues and a gradual decrease in VP activity, suggesting an inhibitory interaction in which elevated VS activity dampens VP output to limit initiation. The slower VP dynamics may reflect a process by which aversive signals are gradually integrated to influence the motivational state. Together, these results identify the VS-VP pathway as a key circuit by which aversive contexts suppress effort-based behavioral initiation, highlighting it as a potential target for treating motivational deficits in depression and schizophrenia.

在令人厌恶的情况下,动机往往会减弱。临床上,动机缺陷与抑郁症和精神分裂症等精神疾病有关,但厌恶环境抑制动机的神经机制尚不清楚。尽管经典理论将动机与结果的期望值联系在一起,但人们对控制基于努力的行为启动的神经回路知之甚少。为了解决这个问题,我们使用方法回避(Ap-Av)任务将动机驱动从目标评估中分离出来,在这个任务中,猕猴评估了奖励和惩罚(向脸上吹气)的结果。作为对照,我们采用了一个完全基于奖励的方法-方法(Ap-Ap)任务。通过化学发生操作,我们发现选择性抑制腹侧纹状体到腹侧苍白球(VS-VP)通路恢复了Ap-Av任务中启动试验的动机,而不影响目标评估。在Ap-Ap任务中未观察到任何影响。这些发现提供了因果证据,证明VS-VP通路介导了厌恶情境中的动机抑制。电生理记录显示VS对厌恶信号的快速反应和VP活性的逐渐降低,表明VS活性升高抑制VP输出以限制起始的抑制相互作用。较慢的VP动态可能反映了厌恶信号逐渐被整合以影响动机状态的过程。总之,这些结果确定了VS-VP通路是厌恶环境抑制基于努力的行为启动的关键回路,强调了它是治疗抑郁症和精神分裂症动机缺陷的潜在目标。
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引用次数: 0
Interplay between syllable duration and pitch during whistle matching in wild nightingales. 野生夜莺口哨匹配过程中音节持续时间和音高的相互作用。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-12 DOI: 10.1016/j.cub.2025.12.025
Juan Sebastián Calderón-García, Giacomo Costalunga, Tim P Vogels, Daniela Vallentin

During complex vocal interactions, different features of acoustic stimuli are integrated to produce appropriate vocal responses,1 such as copying sounds during vocal matching behavior in some animals.2,3,4,5,6,7,8,9,10,11,12 However, little is known about the interplay and possible trade-offs between the different temporal and spectral acoustic features during these vocal exchanges.2,13,14 Nightingales can flexibly match the pitch of their tonal "whistle songs" in real time during counter-singing duels.15,16 Here, we show that the syllable duration of whistle playbacks could alter the song responses of wild nightingales, causing their whistle duration distribution to shift toward the presented stimulus duration. When exposed to whistle playbacks featuring unnatural combinations of pitch and duration, nightingales demonstrate a flexible trade-off between pitch matching and temporal imitation, yet they are constrained by their vocal repertoire. They selectively adapted their vocal responses to approximate these novel stimuli, aligning them with their natural whistle repertoire. We developed a computational model of nightingale whistle-matching behavior that revealed a hierarchical organization of acoustic feature production. During whistle matching, the feature integration process is constrained by the duration of syllables, and pitch matching follows within this temporal framework, forcing a trade-off between the two features. Our findings reveal a complex interplay between the spectral and temporal domains that shapes song-matching behavior.

在复杂的声音相互作用中,声音刺激的不同特征被整合以产生适当的声音反应,例如一些动物在声音匹配行为中复制声音。2,3,4,5,6,7,8,9,10,11,12然而,在这些声音交换过程中,不同时间和频谱声学特征之间的相互作用和可能的权衡知之甚少夜莺可以在对唱决斗中灵活地实时匹配它们的音调“哨子歌”在这里,我们证明了哨声播放的音节持续时间可以改变野生夜莺的鸣叫反应,导致它们的哨声持续时间分布向呈现的刺激持续时间转移。当夜莺被暴露在以音调和持续时间的不自然组合为特征的哨声回放时,夜莺表现出在音调匹配和时间模仿之间的灵活权衡,但它们受到声音曲目的限制。他们有选择地调整自己的声音反应来接近这些新的刺激,使它们与自然的哨声曲目保持一致。我们开发了一个夜莺哨声匹配行为的计算模型,揭示了声学特征产生的分层组织。在哨音匹配过程中,特征整合过程受到音节持续时间的限制,而音高匹配遵循这个时间框架,迫使两个特征之间进行权衡。我们的发现揭示了形成歌曲匹配行为的谱域和时间域之间复杂的相互作用。
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引用次数: 0
Spef1 is a microvillar component that limits apical actomyosin contractility and preserves intestinal barrier function. Spef1是一种微绒毛成分,它限制了顶端肌动球蛋白的收缩,保持了肠屏障功能。
IF 7.5 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2026-02-02 Epub Date: 2026-01-16 DOI: 10.1016/j.cub.2025.12.011
Rocio Tapia, Angelo Morales, Gail A Hecht, Matthew J Tyska

Epithelial sheet integrity is established by adherent contacts that form between cells at the interface between their apical and basolateral domains. Although cell contacts are reinforced by actomyosin contractility, which generates tension that propagates across the apical surface, how epithelial cells tune tension to reinforce junctions without compromising their physical barrier properties remains unclear. Herein, we report that Sperm Flagellar 1 (Spef1) is a microvillar component enriched in the apical domain and terminal web of enterocytes that prevents actomyosin hypercontractility. The loss of function of Spef1 in Caco-2 BBE cells induced invaginations of the apical domain at tricellular contacts, with a redistribution of the tricellular and tight junction components. These changes were driven by an increase in the NM2A:NM2C heavy chain ratio, which elevated tension throughout the apical surface and ultimately compromised barrier function. These findings highlight Spef1 as a microvillar resident that tunes actomyosin contractility across the apical surface to a level appropriate for junctional reinforcement and maintenance of epithelial function.

上皮片的完整性是通过细胞间的贴壁接触建立的,这种接触形成于细胞顶域和底外侧域之间的界面。虽然细胞接触是通过肌动球蛋白的收缩性来加强的,这种收缩性产生的张力在细胞顶端表面传播,但上皮细胞如何调节张力来加强连接而不损害其物理屏障特性仍不清楚。在此,我们报道精子鞭毛1 (Spef1)是一种微绒毛成分,富集于肠细胞的顶端结构域和末端网,可防止肌动球蛋白过度收缩。Spef1在Caco-2 BBE细胞中的功能缺失导致三细胞接触处的顶域内陷,并导致三细胞和紧密连接成分的重新分布。这些变化是由NM2A:NM2C重链比的增加所驱动的,这增加了整个根尖表面的张力,最终损害了屏障功能。这些发现强调了Spef1作为微绒毛居民,调节肌动球蛋白在根尖表面的收缩力,使其达到适当的水平,以加强连接和维持上皮功能。
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引用次数: 0
期刊
Current Biology
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