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PUFFFIN: an ultra-bright, customisable, single-plasmid system for labelling cell neighbourhoods. PUFFFIN:用于标记细胞邻域的超亮、可定制的单质粒系统。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-12 DOI: 10.1038/s44318-024-00154-w
Tamina Lebek, Mattias Malaguti, Giulia Lm Boezio, Lida Zoupi, James Briscoe, Alistair Elfick, Sally Lowell

Cell communication coordinates developmental processes, maintains homeostasis, and contributes to disease. Therefore, understanding the relationship between cells in a shared environment is crucial. Here we introduce Positive Ultra-bright Fluorescent Fusion For Identifying Neighbours (PUFFFIN), a cell neighbour-labelling system based upon secretion and uptake of positively supercharged fluorescent protein s36GFP. We fused s36GFP to mNeonGreen or to a HaloTag, facilitating ultra-bright, sensitive, colour-of-choice labelling. Secretor cells transfer PUFFFIN to neighbours while retaining nuclear mCherry, making identification, isolation, and investigation of live neighbours straightforward. PUFFFIN can be delivered to cells, tissues, or embryos on a customisable single-plasmid construct composed of interchangeable components with the option to incorporate any transgene. This versatility enables the manipulation of cell properties, while simultaneously labelling surrounding cells, in cell culture or in vivo. We use PUFFFIN to ask whether pluripotent cells adjust the pace of differentiation to synchronise with their neighbours during exit from naïve pluripotency. PUFFFIN offers a simple, sensitive, customisable approach to profile non-cell-autonomous responses to natural or induced changes in cell identity or behaviour.

细胞通讯可协调发育过程、维持体内平衡并导致疾病。因此,了解共享环境中细胞之间的关系至关重要。在这里,我们介绍了一种基于正超电荷荧光蛋白 s36GFP 的分泌和吸收的细胞邻居标记系统--正超亮荧光融合识别邻居(PUFFFIN)。我们将 s36GFP 与 mNeonGreen 或 HaloTag 融合,从而实现了超亮、灵敏、颜色可选的标记。分泌细胞将 PUFFFIN 传递给邻近细胞,同时保留核 mCherry,这样就能直接识别、分离和研究活的邻近细胞。PUFFFIN 可以通过一个可定制的单质粒构建体输送到细胞、组织或胚胎中,该构建体由可互换的组件组成,并可选择加入任何转基因。这种多功能性使我们能够在细胞培养或体内操纵细胞特性,同时标记周围的细胞。我们利用 PUFFFIN 来探究多能细胞在脱离幼稚多能性过程中是否会调整分化速度,以便与周围细胞同步。PUFFFIN 提供了一种简单、灵敏、可定制的方法,用于分析细胞对自然或诱导的细胞特性或行为变化的非自主反应。
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引用次数: 0
Structural insights into the molecular effects of the anthelmintics monepantel and betaine on the Caenorhabditis elegans acetylcholine receptor ACR-23. 抗蠕虫药莫奈潘特尔和甜菜碱对优雅尾线虫乙酰胆碱受体 ACR-23 分子影响的结构性启示。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-15 DOI: 10.1038/s44318-024-00165-7
Fenglian Liu, Tianyu Li, Huihui Gong, Fei Tian, Yan Bai, Haowei Wang, Chonglin Yang, Yang Li, Fei Guo, Sheng Liu, Qingfeng Chen

Anthelmintics are drugs used for controlling pathogenic helminths in animals and plants. The natural compound betaine and the recently developed synthetic compound monepantel are both anthelmintics that target the acetylcholine receptor ACR-23 and its homologs in nematodes. Here, we present cryo-electron microscopy structures of ACR-23 in apo, betaine-bound, and betaine- and monepantel-bound states. We show that ACR-23 forms a homo-pentameric channel, similar to some other pentameric ligand-gated ion channels (pLGICs). While betaine molecules are bound to the classical neurotransmitter sites in the inter-subunit interfaces in the extracellular domain, monepantel molecules are bound to allosteric sites formed in the inter-subunit interfaces in the transmembrane domain of the receptor. Although the pore remains closed in betaine-bound state, monepantel binding results in an open channel by wedging into the cleft between the transmembrane domains of two neighboring subunits, which causes dilation of the ion conduction pore. By combining structural analyses with site-directed mutagenesis, electrophysiology and in vivo locomotion assays, we provide insights into the mechanism of action of the anthelmintics monepantel and betaine.

抗蠕虫药是用于控制动物和植物中致病蠕虫的药物。天然化合物甜菜碱和最近开发的合成化合物莫奈潘特尔都是针对线虫体内乙酰胆碱受体 ACR-23 及其同源物的抗蠕虫药。在这里,我们展示了ACR-23在apo、与甜菜碱结合以及与甜菜碱和莫奈潘特尔结合状态下的冷冻电镜结构。我们发现,ACR-23 形成了一个同源五聚体通道,类似于其他一些五聚体配体门控离子通道(pLGIC)。甜菜碱分子与细胞外结构域亚基间界面上的经典神经递质位点结合,而莫奈潘特尔分子则与受体跨膜结构域亚基间界面上形成的异构位点结合。虽然在甜菜碱结合状态下孔道仍处于关闭状态,但莫奈潘特尔结合后会楔入两个相邻亚基的跨膜结构域之间的裂隙,从而导致离子传导孔道扩张,从而形成开放通道。通过将结构分析与定点突变、电生理学和体内运动试验相结合,我们深入了解了杀虫药莫奈潘特尔和甜菜碱的作用机制。
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引用次数: 0
Modular control of vertebrate axis segmentation in time and space. 脊椎动物轴分节在时间和空间上的模块化控制
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-08-09 DOI: 10.1038/s44318-024-00186-2
Ali Seleit, Ian Brettell, Tomas Fitzgerald, Carina Vibe, Felix Loosli, Joachim Wittbrodt, Kiyoshi Naruse, Ewan Birney, Alexander Aulehla

How the timing of development is linked to organismal size is a longstanding question. Although numerous studies have reported a correlation of temporal and spatial traits, the developmental or selective constraints underlying this link remain largely unexplored. We address this question by studying the periodic process of embryonic axis segmentation in-vivo in Oryzias fish. Interspecies comparisons reveal that the timing of segmentation correlates to segment, tissue and organismal size. Segment size in turn scales according to tissue and organism size. To probe for underlying causes, we genetically hybridised two closely related species. Quantitative analysis in ~600 phenotypically diverse F2 embryos reveals a decoupling of timing from size control, while spatial scaling is preserved. Using developmental quantitative trait loci (devQTL) mapping we identify distinct genetic loci linked to either the control of segmentation timing or tissue size. This study demonstrates that a developmental constraint mechanism underlies spatial scaling of axis segmentation, while its spatial and temporal control are dissociable modules.

发育时间如何与生物体大小相关是一个长期存在的问题。尽管许多研究都报道了时间和空间特征的相关性,但这一联系背后的发育或选择性制约因素在很大程度上仍未得到探讨。为了解决这个问题,我们研究了鹗鱼体内胚胎轴分节的周期性过程。种间比较显示,轴的分节时间与分节、组织和生物体的大小相关。节段大小又与组织和生物体大小相关。为了探究其根本原因,我们对两个密切相关的物种进行了基因杂交。对大约 600 个表型不同的 F2 胚胎进行的定量分析显示,时间与大小控制脱钩,而空间比例保持不变。利用发育定量性状位点(devQTL)图谱,我们确定了与分割时间控制或组织大小控制相关的不同遗传位点。这项研究表明,轴分割的空间缩放是发育约束机制的基础,而其空间和时间控制则是可分离的模块。
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引用次数: 0
Identification of BiP as a temperature sensor mediating temperature-induced germline sex reversal in C. elegans. 鉴定 BiP 作为温度传感器介导温度诱导的秀丽隐杆线虫种系性别逆转。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-08-12 DOI: 10.1038/s44318-024-00197-z
Jing Shi, Danli Sheng, Jie Guo, Fangyuan Zhou, Shaofeng Wu, Hongyun Tang

Sex determination in animals is not only determined by karyotype but can also be modulated by environmental cues like temperature via unclear transduction mechanisms. Moreover, in contrast to earlier views that sex may exclusively be determined by either karyotype or temperature, recent observations suggest that these factors rather co-regulate sex, posing another mechanistic mystery. Here, we discovered that certain wild-isolated and mutant C. elegans strains displayed genotypic germline sex determination (GGSD), but with a temperature-override mechanism. Further, we found that BiP, an ER chaperone, transduces temperature information into a germline sex-governing signal, thereby enabling the coexistence of GGSD and temperature-dependent germline sex determination (TGSD). At the molecular level, increased ER protein-folding requirements upon increased temperatures lead to BiP sequestration, resulting in ERAD-dependent degradation of the oocyte fate-driving factor, TRA-2, thus promoting male germline fate. Remarkably, experimentally manipulating BiP or TRA-2 expression allows to switch between GGSD and TGSD. Physiologically, TGSD allows C. elegans hermaphrodites to maintain brood size at warmer temperatures. Moreover, BiP can also influence germline sex determination in a different, non-hermaphroditic nematode species. Collectively, our findings identify thermosensitive BiP as a conserved temperature sensor in TGSD, and provide mechanistic insights into the transition between GGSD and TGSD.

动物的性别决定不仅由核型决定,还可以通过不明确的传导机制受温度等环境线索的调节。此外,与早期认为性别可能完全由核型或温度决定的观点不同,最近的观察表明,这些因素反而共同调控性别,提出了另一个机理之谜。在这里,我们发现某些野生分离株和突变株的秀丽隐杆线虫表现出基因型生殖系性别决定(GGSD),但具有温度覆盖机制。此外,我们还发现ER伴侣蛋白BiP能将温度信息转化为种系性别控制信号,从而使GGSD和温度依赖性种系性别决定(TGSD)共存。在分子水平上,温度升高对ER蛋白折叠的要求增加,导致BiP螯合,导致ERAD依赖性地降解卵母细胞命运驱动因子TRA-2,从而促进雄性生殖系的命运。值得注意的是,通过实验操纵 BiP 或 TRA-2 的表达可以在 GGSD 和 TGSD 之间切换。从生理学角度看,TGSD能让优雅雌雄同体在较高温度下保持育雏规模。此外,在不同的非雌雄同体线虫物种中,BiP 也能影响生殖细胞的性别决定。总之,我们的研究发现热敏性 BiP 是 TGSD 中一种保守的温度传感器,并为 GGSD 和 TGSD 之间的转变提供了机理上的见解。
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引用次数: 0
Loss of Elp3 blocks intestinal tuft cell differentiation via an mTORC1-Atf4 axis. Elp3的缺失会通过mTORC1-Atf4轴阻碍肠簇细胞的分化。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-31 DOI: 10.1038/s44318-024-00184-4
Caroline Wathieu, Arnaud Lavergne, Xinyi Xu, Marion Rolot, Ivan Nemazanyy, Kateryna Shostak, Najla El Hachem, Chloé Maurizy, Charlotte Leemans, Pierre Close, Laurent Nguyen, Christophe Desmet, Sylvia Tielens, Benjamin G Dewals, Alain Chariot

Intestinal tuft cells are critical for anti-helminth parasite immunity because they produce IL-25, which triggers IL-13 secretion by activated group 2 innate lymphoid cells (ILC2s) to expand both goblet and tuft cells. We show that epithelial Elp3, a tRNA-modifying enzyme, promotes tuft cell differentiation and is consequently critical for IL-25 production, ILC2 activation, goblet cell expansion and control of Nippostrongylus brasiliensis helminth infection in mice. Elp3 is essential for the generation of intestinal immature tuft cells and for the IL-13-dependent induction of glycolytic enzymes such as Hexokinase 1 and Aldolase A. Importantly, loss of epithelial Elp3 in the intestine blocks the codon-dependent translation of the Gator1 subunit Nprl2, an mTORC1 inhibitor, which consequently enhances mTORC1 activation and stabilizes Atf4 in progenitor cells. Likewise, Atf4 overexpression in mouse intestinal epithelium blocks tuft cell differentiation in response to intestinal helminth infection. Collectively, our data define Atf4 as a negative regulator of tuft cells and provide insights into promotion of intestinal type 2 immune response to parasites through tRNA modifications.

肠绒毛细胞对于抗蠕虫寄生虫免疫至关重要,因为它们能产生 IL-25,而 IL-25 能触发活化的第 2 组先天性淋巴细胞(ILC2)分泌 IL-13,从而扩增鹅口疮细胞和绒毛细胞。我们的研究表明,上皮细胞 Elp3 是一种 tRNA 修饰酶,它能促进簇细胞分化,因此对 IL-25 的产生、ILC2 的活化、鹅口疮细胞的扩增以及控制小鼠的巴西镍颚线虫感染至关重要。重要的是,肠道上皮细胞 Elp3 的缺失会阻止 Gator1 亚基 Nprl2(一种 mTORC1 抑制剂)的密码依赖性翻译,从而增强 mTORC1 的激活并稳定祖细胞中的 Atf4。同样,Atf4在小鼠肠上皮细胞中的过表达也会阻止簇细胞对肠道蠕虫感染的分化。总之,我们的数据确定了 Atf4 是簇细胞的负调控因子,并为通过 tRNA 修饰促进肠道对寄生虫的 2 型免疫反应提供了见解。
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引用次数: 0
Reactive oxygen species activate the Drosophila TNF receptor Wengen for damage-induced regeneration. 活性氧激活果蝇 TNF 受体 Wengen,促进损伤诱导的再生。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-17 DOI: 10.1038/s44318-024-00155-9
José Esteban-Collado, Mar Fernández-Mañas, Manuel Fernández-Moreno, Ignacio Maeso, Montserrat Corominas, Florenci Serras

Tumor necrosis factor receptors (TNFRs) control pleiotropic pro-inflammatory functions that range from apoptosis to cell survival. The ability to trigger a particular function will depend on the upstream cues, association with regulatory complexes, and downstream pathways. In Drosophila melanogaster, two TNFRs have been identified, Wengen (Wgn) and Grindelwald (Grnd). Although several reports associate these receptors with JNK-dependent apoptosis, it has recently been found that Wgn activates a variety of other functions. We demonstrate that Wgn is required for survival by protecting cells from apoptosis. This is mediated by dTRAF1 and results in the activation of p38 MAP kinase. Remarkably, Wgn is required for apoptosis-induced regeneration and is activated by the reactive oxygen species (ROS) produced following apoptosis. This ROS activation is exclusive for Wgn, but not for Grnd, and can occur after knocking down Eiger/TNFα. The extracellular cysteine-rich domain of Grnd is much more divergent than that of Wgn, which is more similar to TNFRs from other animals, including humans. Our results show a novel TNFR function that responds to stressors by ensuring p38-dependent regeneration.

肿瘤坏死因子受体(TNFR)控制着从细胞凋亡到细胞存活的多种促炎功能。触发特定功能的能力取决于上游线索、与调控复合物的关联以及下游途径。在黑腹果蝇中,发现了两种 TNFR 受体,即 Wengen(Wgn)和 Grindelwald(Grnd)。尽管一些报道称这些受体与依赖于 JNK 的细胞凋亡有关,但最近发现 Wgn 还能激活多种其他功能。我们证明,Wgn 是保护细胞免于凋亡的生存所必需的。这是由 dTRAF1 介导的,并导致 p38 MAP 激酶的激活。值得注意的是,Wgn 是细胞凋亡诱导再生所必需的,并被细胞凋亡后产生的活性氧(ROS)激活。这种 ROS 激活对 Wgn 而言是唯一的,但对 Grnd 则不是,而且在敲除 Eiger/TNFα 后也会发生。与Wgn相比,Grnd的富半胱氨酸胞外结构域差异更大,而Wgn与其他动物(包括人类)的TNFR更相似。我们的研究结果表明了一种新的TNFR功能,它通过确保p38依赖性再生来应对压力。
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引用次数: 0
Wengen's hidden powers: ROS triggers a TNFR-dependent tissue regenerative pathway in Drosophila. 翁根的隐藏力量:ROS 触发果蝇体内依赖 TNFR 的组织再生途径
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-17 DOI: 10.1038/s44318-024-00170-w
Ditte S Andersen, Julien Colombani
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引用次数: 0
CMG helicase disassembly is essential and driven by two pathways in budding yeast. 在芽殖酵母中,CMG 螺旋酶的分解是必不可少的,并由两种途径驱动。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-07-22 DOI: 10.1038/s44318-024-00161-x
Cristian Polo Rivera, Tom D Deegan, Karim P M Labib

The CMG helicase is the stable core of the eukaryotic replisome and is ubiquitylated and disassembled during DNA replication termination. Fungi and animals use different enzymes to ubiquitylate the Mcm7 subunit of CMG, suggesting that CMG ubiquitylation arose repeatedly during eukaryotic evolution. Until now, it was unclear whether cells also have ubiquitin-independent pathways for helicase disassembly and whether CMG disassembly is essential for cell viability. Using reconstituted assays with budding yeast CMG, we generated the mcm7-10R allele that compromises ubiquitylation by SCFDia2. mcm7-10R delays helicase disassembly in vivo, driving genome instability in the next cell cycle. These data indicate that defective CMG ubiquitylation explains the major phenotypes of cells lacking Dia2. Notably, the viability of mcm7-10R and dia2∆ is dependent upon the related Rrm3 and Pif1 DNA helicases that have orthologues in all eukaryotes. We show that Rrm3 acts during S-phase to disassemble old CMG complexes from the previous cell cycle. These findings indicate that CMG disassembly is essential in yeast cells and suggest that Pif1-family helicases might have mediated CMG disassembly in ancestral eukaryotes.

CMG螺旋酶是真核生物复制体的稳定核心,在DNA复制终止时被泛素化和分解。真菌和动物使用不同的酶对CMG的Mcm7亚基进行泛素化,这表明CMG泛素化在真核生物进化过程中反复出现。直到现在,人们还不清楚细胞是否也有不依赖泛素的螺旋酶分解途径,也不清楚CMG分解是否是细胞存活的必要条件。我们利用芽殖酵母 CMG 的重组实验,产生了 mcm7-10R 等位基因,它损害了 SCFDia2 的泛素化作用。mcm7-10R 在体内延迟了螺旋酶的分解,导致下一个细胞周期中基因组的不稳定性。这些数据表明,CMG泛素化缺陷解释了缺乏Dia2的细胞的主要表型。值得注意的是,mcm7-10R 和 dia2∆ 的活力依赖于相关的 Rrm3 和 Pif1 DNA 螺旋酶,它们在所有真核生物中都有直向同源物。我们发现,Rrm3 在 S 期的作用是分解上一个细胞周期的旧 CMG 复合物。这些发现表明,CMG的分解在酵母细胞中是必不可少的,并表明Pif1家族螺旋酶可能在真核生物的祖先中介导了CMG的分解。
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引用次数: 0
Lysosomal TBK1 responds to amino acid availability to relieve Rab7-dependent mTORC1 inhibition. 溶酶体 TBK1 对氨基酸的可用性做出反应,以缓解 Rab7 依赖性 mTORC1 的抑制作用。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-08-05 DOI: 10.1038/s44318-024-00180-8
Gabriel Talaia, Amanda Bentley-DeSousa, Shawn M Ferguson

Lysosomes play a pivotal role in coordinating macromolecule degradation and regulating cell growth and metabolism. Despite substantial progress in identifying lysosomal signaling proteins, understanding the pathways that synchronize lysosome functions with changing cellular demands remains incomplete. This study uncovers a role for TANK-binding kinase 1 (TBK1), well known for its role in innate immunity and organelle quality control, in modulating lysosomal responsiveness to nutrients. Specifically, we identify a pool of TBK1 that is recruited to lysosomes in response to elevated amino acid levels. This lysosomal TBK1 phosphorylates Rab7 on serine 72. This is critical for alleviating Rab7-mediated inhibition of amino acid-dependent mTORC1 activation. Furthermore, a TBK1 mutant (E696K) associated with amyotrophic lateral sclerosis and frontotemporal dementia constitutively accumulates at lysosomes, resulting in elevated Rab7 phosphorylation and increased mTORC1 activation. This data establishes the lysosome as a site of amino acid regulated TBK1 signaling that is crucial for efficient mTORC1 activation. This lysosomal pool of TBK1 has broader implications for lysosome homeostasis, and its dysregulation could contribute to the pathogenesis of ALS-FTD.

溶酶体在协调大分子降解以及调节细胞生长和新陈代谢方面发挥着关键作用。尽管在鉴定溶酶体信号蛋白方面取得了重大进展,但对使溶酶体功能与不断变化的细胞需求同步的途径的了解仍然不全面。本研究发现了 TANK 结合激酶 1(TBK1)在调节溶酶体对营养物质的反应能力方面的作用,TBK1 因其在先天性免疫和细胞器质量控制中的作用而广为人知。具体来说,我们发现了一个 TBK1 池,它在氨基酸水平升高时被招募到溶酶体。这种溶酶体 TBK1 会使 Rab7 的丝氨酸 72 磷酸化。这对于减轻 Rab7 介导的氨基酸依赖性 mTORC1 激活的抑制作用至关重要。此外,一种与肌萎缩性侧索硬化症和额颞叶痴呆症相关的 TBK1 突变体(E696K)会在溶酶体中蓄积,导致 Rab7 磷酸化升高和 mTORC1 激活增加。这一数据证实溶酶体是氨基酸调控 TBK1 信号的场所,对有效激活 mTORC1 至关重要。这种溶酶体 TBK1 池对溶酶体的稳态具有更广泛的意义,它的失调可能导致 ALS-FTD 的发病机制。
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引用次数: 0
PQBP3 prevents senescence by suppressing PSME3-mediated proteasomal Lamin B1 degradation. PQBP3 通过抑制 PSME3 介导的蛋白酶体 Lamin B1 降解来防止衰老。
IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-01 Epub Date: 2024-08-05 DOI: 10.1038/s44318-024-00192-4
Yuki Yoshioka, Yong Huang, Xiaocen Jin, Kien Xuan Ngo, Tomohiro Kumaki, Meihua Jin, Saori Toyoda, Sumire Takayama, Maiko Inotsume, Kyota Fujita, Hidenori Homma, Toshio Ando, Hikari Tanaka, Hitoshi Okazawa

Senescence of nondividing neurons remains an immature concept, with especially the regulatory molecular mechanisms of senescence-like phenotypes and the role of proteins associated with neurodegenerative diseases in triggering neuronal senescence remaining poorly explored. In this study, we reveal that the nucleolar polyglutamine binding protein 3 (PQBP3; also termed NOL7), which has been linked to polyQ neurodegenerative diseases, regulates senescence as a gatekeeper of cytoplasmic DNA leakage. PQBP3 directly binds PSME3 (proteasome activator complex subunit 3), a subunit of the 11S proteasome regulator complex, decreasing PSME3 interaction with Lamin B1 and thereby preventing Lamin B1 degradation and senescence. Depletion of endogenous PQBP3 causes nuclear membrane instability and release of genomic DNA from the nucleus to the cytosol. Among multiple tested polyQ proteins, ataxin-1 (ATXN1) partially sequesters PQBP3 to inclusion bodies, reducing nucleolar PQBP3 levels. Consistently, knock-in mice expressing mutant Atxn1 exhibit decreased nuclear PQBP3 and a senescence phenotype in Purkinje cells of the cerebellum. Collectively, these results suggest homologous roles of the nucleolar protein PQBP3 in cellular senescence and neurodegeneration.

非分裂神经元的衰老仍然是一个不成熟的概念,尤其是衰老样表型的调控分子机制以及与神经退行性疾病相关的蛋白质在引发神经元衰老中的作用仍然没有得到充分的探讨。在这项研究中,我们揭示了与多Q神经退行性疾病相关的核小体多谷氨酰胺结合蛋白3(PQBP3;又称NOL7)作为细胞质DNA泄漏的守门员调控衰老。PQBP3 可直接与 11S 蛋白酶体调节复合体的一个亚基 PSME3(蛋白酶体激活复合体亚基 3)结合,减少 PSME3 与 Lamin B1 的相互作用,从而防止 Lamin B1 降解和衰老。消耗内源性 PQBP3 会导致核膜不稳定,基因组 DNA 从细胞核释放到细胞质。在多种测试过的多Q蛋白中,共济失调蛋白-1(ATXN1)能将PQBP3部分封存到包涵体中,从而降低核仁PQBP3的水平。同样,表达突变体 Atxn1 的基因敲入小鼠表现出核 PQBP3 减少和小脑浦肯野细胞衰老表型。总之,这些结果表明核极蛋白PQBP3在细胞衰老和神经退行性变中具有同源作用。
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引用次数: 0
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