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T cells use focal adhesions to pull themselves through confined environments. T 细胞利用病灶粘附力使自己穿过封闭的环境。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-06-18 DOI: 10.1083/jcb.202310067
Alexia Caillier, David Oleksyn, Deborah J Fowell, Jim Miller, Patrick W Oakes

Immune cells are highly dynamic and able to migrate through environments with diverse biochemical and mechanical compositions. Their migration has classically been defined as amoeboid under the assumption that it is integrin independent. Here, we show that activated primary Th1 T cells require both confinement and extracellular matrix proteins to migrate efficiently. This migration is mediated through small and dynamic focal adhesions that are composed of the same proteins associated with canonical mesenchymal cell focal adhesions, such as integrins, talin, and vinculin. These focal adhesions, furthermore, localize to sites of contractile traction stresses, enabling T cells to pull themselves through confined spaces. Finally, we show that Th1 T cells preferentially follow tracks of other T cells, suggesting that these adhesions modify the extracellular matrix to provide additional environmental guidance cues. These results demonstrate not only that the boundaries between amoeboid and mesenchymal migration modes are ambiguous, but that integrin-mediated focal adhesions play a key role in T cell motility.

免疫细胞具有高度动态性,能够在具有不同生化和机械成分的环境中迁移。根据独立于整合素的假设,它们的迁移通常被定义为非膜性迁移。在这里,我们发现活化的原发性 Th1 T 细胞需要封闭和细胞外基质蛋白才能有效迁移。这种迁移是通过小而动态的局灶粘附介导的,局灶粘附由与典型间充质细胞局灶粘附相关的相同蛋白组成,如整合素、塔林和长链蛋白。此外,这些局灶粘附还定位在收缩牵引应力的部位,使 T 细胞能将自己拉过狭窄的空间。最后,我们发现 Th1 T 细胞会优先追随其他 T 细胞的轨迹,这表明这些粘附改变了细胞外基质,从而提供了额外的环境引导线索。这些结果不仅证明了非变形和间质迁移模式之间的界限模糊不清,而且证明了整合素介导的局灶粘附在 T 细胞运动中起着关键作用。
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引用次数: 0
Calorie restriction activates a gastric Notch-FOXO1 pathway to expand ghrelin cells. 卡路里限制会激活胃 Notch-FOXO1 通路,从而扩大胃泌素细胞。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-03 DOI: 10.1083/jcb.202305093
Wendy M McKimpson, Sophia Spiegel, Maria Mukhanova, Michael Kraakman, Wen Du, Takumi Kitamoto, Junjie Yu, Zhaobin Deng, Utpal Pajvani, Domenico Accili

Calorie restriction increases lifespan. Among the tissue-specific protective effects of calorie restriction, the impact on the gastrointestinal tract remains unclear. We report increased numbers of chromogranin A-positive (+), including orexigenic ghrelin+ cells, in the stomach of calorie-restricted mice. This effect was accompanied by increased Notch target Hes1 and Notch ligand Jag1 and was reversed by blocking Notch with DAPT, a gamma-secretase inhibitor. Primary cultures and genetically modified reporter mice show that increased endocrine cell abundance is due to altered Lgr5+ stem and Neurog3+ endocrine progenitor cell proliferation. Different from the intestine, calorie restriction decreased gastric Lgr5+ stem cells, while increasing a FOXO1/Neurog3+ subpopulation of endocrine progenitors in a Notch-dependent manner. Further, activation of FOXO1 was sufficient to promote endocrine cell differentiation independent of Notch. The Notch inhibitor PF-03084014 or ghrelin receptor antagonist GHRP-6 reversed the phenotypic effects of calorie restriction in mice. Tirzepatide additionally expanded ghrelin+ cells in mice. In summary, calorie restriction promotes Notch-dependent, FOXO1-regulated gastric endocrine cell differentiation.

限制卡路里摄入会延长寿命。在卡路里限制对特定组织的保护作用中,对胃肠道的影响仍不清楚。我们报告了限制卡路里摄入的小鼠胃中嗜铬粒蛋白 A 阳性(+)细胞数量的增加,其中包括嗜食性胃泌素+细胞。这种效应伴随着Notch靶标Hes1和Notch配体Jag1的增加,并通过使用γ-分泌酶抑制剂DAPT阻断Notch而逆转。原代培养物和转基因报告小鼠表明,内分泌细胞数量的增加是由于Lgr5+干细胞和Neurog3+内分泌祖细胞增殖的改变。与肠道不同的是,卡路里限制减少了胃Lgr5+干细胞,而内分泌祖细胞的FOXO1/Neurog3+亚群则以Notch依赖性方式增加。此外,FOXO1的激活足以促进独立于Notch的内分泌细胞分化。Notch抑制剂PF-03084014或胃泌素受体拮抗剂GHRP-6可逆转小鼠热量限制的表型效应。替扎帕肽还能扩大小鼠的胃泌素+细胞。总之,卡路里限制促进了Notch依赖性、FOXO1调控的胃内分泌细胞分化。
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引用次数: 0
UBAP2L contributes to formation of P-bodies and modulates their association with stress granules. UBAP2L 有助于 P 型体的形成,并能调节它们与应激颗粒的结合。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-15 DOI: 10.1083/jcb.202307146
Claire L Riggs, Nancy Kedersha, Misheel Amarsanaa, Safiyah Noor Zubair, Pavel Ivanov, Paul Anderson

Stress triggers the formation of two distinct cytoplasmic biomolecular condensates: stress granules (SGs) and processing bodies (PBs), both of which may contribute to stress-responsive translation regulation. Though PBs can be present constitutively, stress can increase their number and size and lead to their interaction with stress-induced SGs. The mechanism of such interaction, however, is largely unknown. Formation of canonical SGs requires the RNA binding protein Ubiquitin-Associated Protein 2-Like (UBAP2L), which is a central SG node protein in the RNA-protein interaction network of SGs and PBs. UBAP2L binds to the essential SG and PB proteins G3BP and DDX6, respectively. Research on UBAP2L has mostly focused on its role in SGs, but not its connection to PBs. We find that UBAP2L is not solely an SG protein but also localizes to PBs in certain conditions, contributes to PB biogenesis and SG-PB interactions, and can nucleate hybrid granules containing SG and PB components in cells. These findings inform a new model for SG and PB formation in the context of UBAP2L's role.

应激会引发两种不同的细胞质生物分子凝聚体的形成:应激颗粒(SGs)和加工体(PBs),它们都可能有助于应激反应翻译调控。虽然 PBs 可组成性存在,但应激可增加它们的数量和大小,并导致它们与应激诱导的 SGs 相互作用。然而,这种相互作用的机制在很大程度上还不清楚。典型 SG 的形成需要 RNA 结合蛋白类泛素相关蛋白 2(Ubiquitin-Associated Protein 2-Like,UBAP2L),它是 SG 与 PB 的 RNA 蛋白相互作用网络中的核心节点蛋白。UBAP2L 分别与重要的 SG 和 PB 蛋白 G3BP 和 DDX6 结合。对 UBAP2L 的研究主要集中在它在 SG 中的作用,而没有关注它与 PB 的联系。我们发现,UBAP2L 不仅仅是一种 SG 蛋白,在某些条件下还会定位到 PB,促进 PB 的生物生成和 SG-PB 的相互作用,并能在细胞中核化含有 SG 和 PB 成分的混合颗粒。这些发现为 UBAP2L 的作用背景下 SG 和 PB 的形成提供了一个新模型。
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引用次数: 0
Dynamic interaction of REEP5-MFN1/2 enables mitochondrial hitchhiking on tubular ER. REEP5-MFN1/2 的动态相互作用使线粒体能够在管状 ER 上搭便车。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-08-12 DOI: 10.1083/jcb.202304031
Shue Chen, Yang Sun, Yuling Qin, Lan Yang, Zhenhua Hao, Zhihao Xu, Mikael Björklund, Wei Liu, Zhi Hong

Mitochondrial functions can be regulated by membrane contact sites with the endoplasmic reticulum (ER). These mitochondria-ER contact sites (MERCs) are functionally heterogeneous and maintained by various tethers. Here, we found that REEP5, an ER tubule-shaping protein, interacts with Mitofusins 1/2 to mediate mitochondrial distribution throughout the cytosol by a new transport mechanism, mitochondrial "hitchhiking" with tubular ER on microtubules. REEP5 depletion led to reduced tethering and increased perinuclear localization of mitochondria. Conversely, increasing REEP5 expression facilitated mitochondrial distribution throughout the cytoplasm. Rapamycin-induced irreversible REEP5-MFN1/2 interaction led to mitochondrial hyperfusion, implying that the dynamic release of mitochondria from tethering is necessary for normal mitochondrial distribution and dynamics. Functionally, disruption of MFN2-REEP5 interaction dynamics by forced dimerization or silencing REEP5 modulated the production of mitochondrial reactive oxygen species (ROS). Overall, our results indicate that dynamic REEP5-MFN1/2 interaction mediates cytosolic distribution and connectivity of the mitochondrial network by "hitchhiking" and this process regulates mitochondrial ROS, which is vital for multiple physiological functions.

线粒体的功能可以通过与内质网(ER)的膜接触点来调节。这些线粒体-ER接触位点(MERCs)在功能上是异质的,由不同的系链维持。在这里,我们发现ER小管塑形蛋白REEP5与Mitofusins 1/2相互作用,通过一种新的运输机制--线粒体在微管上与管状ER "搭便车"--介导线粒体在整个细胞质中的分布。耗尽 REEP5 会导致线粒体的系链减少和核周定位增加。相反,增加 REEP5 的表达则有利于线粒体在整个细胞质中的分布。雷帕霉素诱导的 REEP5-MFN1/2 不可逆相互作用导致线粒体过度融合,这意味着线粒体从系链中动态释放是线粒体正常分布和动态变化的必要条件。从功能上讲,通过强迫二聚化或沉默 REEP5 来破坏 MFN2-REEP5相互作用的动态,可调节线粒体活性氧(ROS)的产生。总之,我们的研究结果表明,REEP5-MFN1/2的动态相互作用通过 "搭便车 "介导线粒体网络的胞浆分布和连接,这一过程调节线粒体ROS,而ROS对多种生理功能至关重要。
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引用次数: 0
A force-sensitive mutation reveals a non-canonical role for dynein in anaphase progression. 力敏感突变揭示了dynein在无丝分裂进程中的非典型作用。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-01 DOI: 10.1083/jcb.202310022
David Salvador-Garcia, Li Jin, Andrew Hensley, Mert Gölcük, Emmanuel Gallaud, Sami Chaaban, Fillip Port, Alessio Vagnoni, Vicente José Planelles-Herrero, Mark A McClintock, Emmanuel Derivery, Andrew P Carter, Régis Giet, Mert Gür, Ahmet Yildiz, Simon L Bullock

The diverse roles of the dynein motor in shaping microtubule networks and cargo transport complicate in vivo analysis of its functions significantly. To address this issue, we have generated a series of missense mutations in Drosophila Dynein heavy chain. We show that mutations associated with human neurological disease cause a range of defects, including impaired cargo trafficking in neurons. We also describe a novel microtubule-binding domain mutation that specifically blocks the metaphase-anaphase transition during mitosis in the embryo. This effect is independent from dynein's canonical role in silencing the spindle assembly checkpoint. Optical trapping of purified dynein complexes reveals that this mutation only compromises motor performance under load, a finding rationalized by the results of all-atom molecular dynamics simulations. We propose that dynein has a novel function in anaphase progression that depends on it operating in a specific load regime. More broadly, our work illustrates how in vivo functions of motors can be dissected by manipulating their mechanical properties.

肌球蛋白马达在塑造微管网络和货物运输方面的作用多种多样,这使得对其功能的体内分析变得非常复杂。为了解决这个问题,我们在果蝇Dynein重链中产生了一系列错义突变。我们发现,与人类神经系统疾病相关的突变会导致一系列缺陷,包括神经元中的货物运输受损。我们还描述了一种新型微管结合域突变,它能特异性地阻断胚胎有丝分裂过程中的移行期-无丝分裂期转变。这种效应与动力蛋白在沉默纺锤体组装检查点中的典型作用无关。对纯化的动力蛋白复合物进行的光学捕获显示,这种突变只在负载条件下影响电机性能,全原子分子动力学模拟的结果也证明了这一发现的合理性。我们提出,dynein 在无丝分裂进程中具有一种新的功能,这种功能取决于它在特定的负载条件下运行。更广泛地说,我们的工作说明了如何通过操纵电机的机械特性来剖析其体内功能。
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引用次数: 0
De novo lipid synthesis and polarized prenylation drive cell invasion through basement membrane. 新的脂质合成和极化的前酰化推动细胞侵入基底膜。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-15 DOI: 10.1083/jcb.202402035
Kieop Park, Aastha Garde, Siddharthan B Thendral, Adam W J Soh, Qiuyi Chi, David R Sherwood

To breach the basement membrane, cells in development and cancer use large, transient, specialized lipid-rich membrane protrusions. Using live imaging, endogenous protein tagging, and cell-specific RNAi during Caenorhabditis elegans anchor cell (AC) invasion, we demonstrate that the lipogenic SREBP transcription factor SBP-1 drives the expression of the fatty acid synthesis enzymes POD-2 and FASN-1 prior to invasion. We show that phospholipid-producing LPIN-1 and sphingomyelin synthase SMS-1, which use fatty acids as substrates, produce lysosome stores that build the AC's invasive protrusion, and that SMS-1 also promotes protrusion localization of the lipid raft partitioning ZMP-1 matrix metalloproteinase. Finally, we discover that HMG-CoA reductase HMGR-1, which generates isoprenoids for prenylation, localizes to the ER and enriches in peroxisomes at the AC invasive front, and that the final transmembrane prenylation enzyme, ICMT-1, localizes to endoplasmic reticulum exit sites that dynamically polarize to deliver prenylated GTPases for protrusion formation. Together, these results reveal a collaboration between lipogenesis and a polarized lipid prenylation system that drives invasive protrusion formation.

为了突破基底膜,细胞在发育和癌变过程中会使用大型、瞬时、特化的富脂膜突起。在秀丽隐杆线虫锚细胞(AC)入侵过程中,我们利用实时成像、内源蛋白标记和细胞特异性 RNAi 技术证明,在入侵之前,脂质生成 SREBP 转录因子 SBP-1 驱动脂肪酸合成酶 POD-2 和 FASN-1 的表达。我们还发现,以脂肪酸为底物的磷脂生产酶 LPIN-1 和鞘磷脂合成酶 SMS-1,可产生溶酶体储存,从而构建 AC 的侵袭性突起,SMS-1 还可促进脂筏分区 ZMP-1 基质金属蛋白酶的突起定位。最后,我们发现,HMG-CoA 还原酶 HMGR-1 能生成用于前炔化的异丙肾上腺素,它能定位到 ER 并富集在 AC 侵袭前沿的过氧物酶体中,最后一种跨膜前炔化酶 ICMT-1 能定位到内质网出口位点,这些位点能动态极化,为突起的形成提供前炔化 GTP 酶。这些结果共同揭示了脂肪生成与极化脂质前酰化系统之间的协作,这种协作推动了侵袭性突起的形成。
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引用次数: 0
Centrosome-organized plasma membrane infoldings linked to growth of a cortical actin domain. 中心体组织的质膜内折与皮质肌动蛋白结构域的生长有关。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-06-27 DOI: 10.1083/jcb.202403115
Rebecca Tam, Tony J C Harris

Regulated cell shape change requires the induction of cortical cytoskeletal domains. Often, local changes to plasma membrane (PM) topography are involved. Centrosomes organize cortical domains and can affect PM topography by locally pulling the PM inward. Are these centrosome effects coupled? At the syncytial Drosophila embryo cortex, centrosome-induced actin caps grow into dome-like compartments for mitoses. We found the nascent cap to be a collection of PM folds and tubules formed over the astral centrosomal MT array. The localized infoldings require centrosome and dynein activities, and myosin-based surface tension prevents them elsewhere. Centrosome-engaged PM infoldings become specifically enriched with an Arp2/3 induction pathway. Arp2/3 actin network growth between the infoldings counterbalances centrosomal pulling forces and disperses the folds for actin cap expansion. Abnormal domain topography with either centrosome or Arp2/3 disruption correlates with decreased exocytic vesicle association. Together, our data implicate centrosome-organized PM infoldings in coordinating Arp2/3 network growth and exocytosis for cortical domain assembly.

调节细胞形状的变化需要诱导皮质细胞骨架结构域。这通常涉及质膜(PM)形貌的局部变化。中心体组织皮质结构域,可通过局部向内拉动质膜来影响质膜的形貌。这些中心体效应是耦合的吗?在合胞果蝇胚胎皮层,中心体诱导的肌动蛋白帽生长为有丝分裂的圆顶状区室。我们发现新生帽是星形中心体 MT 阵列上形成的 PM 褶皱和小管的集合。局部的折叠需要中心体和动力蛋白的活动,而肌球蛋白的表面张力会阻止它们在其他地方形成。中心体参与的PM内陷通过Arp2/3诱导途径变得特别丰富。褶皱之间的 Arp2/3 肌动蛋白网络生长抵消了中心体的拉力,并分散了褶皱以促进肌动蛋白帽的扩张。中心粒或 Arp2/3 中断导致的异常结构域拓扑与外ocytic囊泡结合减少有关。总之,我们的数据表明,中心体组织的 PM 折叠协调了 Arp2/3 网络的生长和皮质结构域组装的外泌作用。
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引用次数: 0
A genome-wide screen links peroxisome regulation with Wnt signaling through RNF146 and TNKS/2. 一项全基因组筛选通过 RNF146 和 TNKS/2 将过氧物酶体调控与 Wnt 信号传导联系起来。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-05 DOI: 10.1083/jcb.202312069
Jonathan T Vu, Katherine U Tavasoli, Connor J Sheedy, Soham P Chowdhury, Lori Mandjikian, Julien Bacal, Meghan A Morrissey, Chris D Richardson, Brooke M Gardner

Peroxisomes are membrane-bound organelles harboring metabolic enzymes. In humans, peroxisomes are required for normal development, yet the genes regulating peroxisome function remain unclear. We performed a genome-wide CRISPRi screen to identify novel factors involved in peroxisomal homeostasis. We found that inhibition of RNF146, an E3 ligase activated by poly(ADP-ribose), reduced the import of proteins into peroxisomes. RNF146-mediated loss of peroxisome import depended on the stabilization and activity of the poly(ADP-ribose) polymerases TNKS and TNKS2, which bind the peroxisomal membrane protein PEX14. We propose that RNF146 and TNKS/2 regulate peroxisome import efficiency by PARsylation of proteins at the peroxisome membrane. Interestingly, we found that the loss of peroxisomes increased TNKS/2 and RNF146-dependent degradation of non-peroxisomal substrates, including the β-catenin destruction complex component AXIN1, which was sufficient to alter the amplitude of β-catenin transcription. Together, these observations not only suggest previously undescribed roles for RNF146 in peroxisomal regulation but also a novel role in bridging peroxisome function with Wnt/β-catenin signaling during development.

过氧物酶体是一种膜结合细胞器,内含代谢酶。人类的正常发育需要过氧物酶体,但调节过氧物酶体功能的基因仍不清楚。我们进行了全基因组 CRISPRi 筛选,以鉴定参与过氧物酶体稳态的新因子。我们发现,抑制 RNF146(一种由聚(ADP-核糖)激活的 E3 连接酶)会减少蛋白质向过氧化物酶体的输入。RNF146 介导的过氧化物酶体导入损失取决于多(ADP-核糖)聚合酶 TNKS 和 TNKS2 的稳定和活性,而 TNKS2 与过氧化物酶体膜蛋白 PEX14 结合。我们认为,RNF146 和 TNKS/2 通过过氧化物酶体膜上蛋白的 PARsylation 来调节过氧化物酶体的导入效率。有趣的是,我们发现过氧化物酶体的缺失增加了 TNKS/2 和 RNF146 对非过氧化物酶体底物的依赖性降解,包括 β-catenin破坏复合体成分 AXIN1,这足以改变 β-catenin转录的幅度。这些观察结果表明,RNF146不仅在过氧化物酶体调控中发挥了以前未曾描述过的作用,而且在发育过程中还在连接过氧化物酶体功能与Wnt/β-catenin信号方面发挥了新的作用。
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引用次数: 0
AMPK activation induces RALDH+ tolerogenic dendritic cells by rewiring glucose and lipid metabolism. AMPK 激活可通过重构葡萄糖和脂质代谢诱导 RALDH+耐受性树突状细胞。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-08-08 DOI: 10.1083/jcb.202401024
Eline C Brombacher, Thiago A Patente, Alwin J van der Ham, Tijmen J A Moll, Frank Otto, Fenne W M Verheijen, Esther A Zaal, Arnoud H de Ru, Rayman T N Tjokrodirijo, Celia R Berkers, Peter A van Veelen, Bruno Guigas, Bart Everts

Dendritic cell (DC) activation and function are underpinned by profound changes in cellular metabolism. Several studies indicate that the ability of DCs to promote tolerance is dependent on catabolic metabolism. Yet the contribution of AMP-activated kinase (AMPK), a central energy sensor promoting catabolism, to DC tolerogenicity remains unknown. Here, we show that AMPK activation renders human monocyte-derived DCs tolerogenic as evidenced by an enhanced ability to drive differentiation of regulatory T cells, a process dependent on increased RALDH activity. This is accompanied by several metabolic changes, including increased breakdown of glycerophospholipids, enhanced mitochondrial fission-dependent fatty acid oxidation, and upregulated glucose catabolism. This metabolic rewiring is functionally important as we found interference with these metabolic processes to reduce to various degrees AMPK-induced RALDH activity as well as the tolerogenic capacity of moDCs. Altogether, our findings reveal a key role for AMPK signaling in shaping DC tolerogenicity and suggest AMPK as a target to direct DC-driven tolerogenic responses in therapeutic settings.

树突状细胞(DC)的活化和功能是由细胞代谢的深刻变化支撑的。一些研究表明,树突状细胞促进耐受的能力取决于分解代谢。然而,促进新陈代谢的中心能量传感器 AMPK 对 DC 耐受性的贡献仍然未知。在这里,我们发现 AMPK 激活可使人类单核细胞衍生的 DC 产生耐受性,这表现在驱动调节性 T 细胞分化的能力增强,而这一过程依赖于 RALDH 活性的增加。与此同时,新陈代谢也发生了一些变化,包括甘油磷脂分解增加、线粒体裂变依赖性脂肪酸氧化增强以及葡萄糖分解代谢上调。这种代谢重构在功能上非常重要,因为我们发现干扰这些代谢过程会在不同程度上降低 AMPK 诱导的 RALDH 活性以及 moDCs 的耐受能力。总之,我们的研究结果揭示了 AMPK 信号在形成直流耐受性中的关键作用,并建议将 AMPK 作为治疗环境中指导直流驱动的耐受性反应的靶点。
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引用次数: 0
An evolutionarily conserved AnkyrinG-dependent motif clusters axonal K2P K+ channels. 轴突 K2P K+ 通道的一个进化保守的 AnkyrinG 依赖性基团。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-07 Epub Date: 2024-07-30 DOI: 10.1083/jcb.202401140
Gabriel Escobedo, Yu Wu, Yuki Ogawa, Xiaoyun Ding, Matthew N Rasband

The evolution of ion channel clustering at nodes of Ranvier enabled the development of complex vertebrate nervous systems. At mammalian nodes, the K+ leak channels TRAAK and TREK-1 underlie membrane repolarization. Despite the molecular similarities between nodes and the axon initial segment (AIS), TRAAK and TREK-1 are reportedly node-specific, suggesting a unique clustering mechanism. However, we show that TRAAK and TREK-1 are enriched at both nodes and AIS through a common mechanism. We identified a motif near the C-terminus of TRAAK that is necessary and sufficient for its clustering. The motif first evolved among cartilaginous fish. Using AnkyrinG (AnkG) conditional knockout mice, CRISPR/Cas9-mediated disruption of AnkG, co-immunoprecipitation, and surface recruitment assays, we show that TRAAK forms a complex with AnkG and that AnkG is necessary for TRAAK's AIS and nodal clustering. In contrast, TREK-1's clustering requires TRAAK. Our results expand the repertoire of AIS and nodal ion channel clustering mechanisms and emphasize AnkG's central role in assembling excitable domains.

兰维耶结点离子通道集群的进化使复杂的脊椎动物神经系统得以发展。在哺乳动物的节点处,K+泄漏通道TRAAK和TREK-1是膜再极化的基础。尽管节点和轴突起始节段(AIS)之间存在分子相似性,但据报道 TRAAK 和 TREK-1 具有节点特异性,这表明它们具有独特的集群机制。然而,我们的研究表明,TRAAK 和 TREK-1 是通过一种共同的机制富集于节点和 AIS 的。我们在 TRAAK 的 C 端附近发现了一个对其聚类十分必要和充分的基团。该基调首先在软骨鱼类中进化。利用AnkyrinG(AnkG)条件性基因敲除小鼠、CRISPR/Cas9介导的AnkG干扰、共免疫沉淀和表面招募试验,我们发现TRAAK与AnkG形成了复合物,并且AnkG是TRAAK的AIS和结节集群所必需的。相反,TREK-1的聚类需要TRAAK。我们的研究结果扩大了AIS和节点离子通道聚类机制的范围,并强调了AnkG在组装可兴奋结构域中的核心作用。
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引用次数: 0
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