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Feedback control of the heat shock response by spatiotemporal regulation of Hsp70. 通过对 Hsp70 的时空调控对热休克反应进行反馈控制。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-09-20 DOI: 10.1083/jcb.202401082
Rania Garde, Annisa Dea, Madeline F Herwig, Asif Ali, David Pincus

Cells maintain homeostasis via dynamic regulation of stress response pathways. Stress pathways transiently induce response regulons via negative feedback loops, but the extent to which individual genes provide feedback has not been comprehensively measured for any pathway. Here, we disrupted the induction of each gene in the Saccharomyces cerevisiae heat shock response (HSR) and quantified cell growth and HSR dynamics following heat shock. The screen revealed a core feedback loop governing the expression of the chaperone Hsp70 reinforced by an auxiliary feedback loop controlling Hsp70 subcellular localization. Mathematical modeling and live imaging demonstrated that multiple HSR targets converge to promote Hsp70 nuclear localization via its release from cytosolic condensates. Following ethanol stress, a distinct set of factors similarly converged on Hsp70, suggesting that nonredundant subsets of the HSR regulon confer feedback under different conditions. Flexible spatiotemporal feedback loops may broadly organize stress response regulons and expand their adaptive capacity.

细胞通过应激反应途径的动态调控来维持稳态。应激通路通过负反馈环路瞬时诱导反应调节子,但尚未对任何通路的单个基因提供反馈的程度进行全面测量。在这里,我们破坏了酿酒酵母热休克反应(HSR)中每个基因的诱导,并量化了热休克后的细胞生长和 HSR 动态。筛选结果显示,一个核心反馈环路控制着伴侣蛋白 Hsp70 的表达,而一个辅助反馈环路控制着 Hsp70 的亚细胞定位。数学建模和实时成像证明,多个HSR靶标通过从细胞膜凝聚物中释放Hsp70,共同促进Hsp70的核定位。乙醇胁迫后,一组不同的因子同样会聚到 Hsp70 上,这表明 HSR 调节子的非冗余子集在不同条件下会产生反馈。灵活的时空反馈回路可以广泛地组织应激反应调控子并扩大其适应能力。
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引用次数: 0
Sec23IP recruits VPS13B/COH1 to ER exit site-Golgi interface for tubular ERGIC formation. Sec23IP 将 VPS13B/COH1 募集到 ER 出口位点-高尔基界面,以形成管状 ERGIC。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-10-01 DOI: 10.1083/jcb.202402083
Yuanjiao Du, Xinyu Fan, Chunyu Song, Weiping Chang, Juan Xiong, Lin Deng, Wei-Ke Ji

VPS13B/COH1 is the only known causative factor for Cohen syndrome, an early-onset autosomal recessive developmental disorder with intellectual inability, developmental delay, joint hypermobility, myopia, and facial dysmorphism as common features, but the molecular basis of VPS13B/COH1 in pathogenesis remains largely unclear. Here, we identify Sec23 interacting protein (Sec23IP) at the ER exit site (ERES) as a VPS13B adaptor that recruits VPS13B to ERES-Golgi interfaces. VPS13B interacts directly with Sec23IP via the VPS13 adaptor binding domain (VAB), and the interaction promotes the association between ERES and the Golgi. Disease-associated missense mutations of VPS13B-VAB impair the interaction with Sec23IP. Knockout of VPS13B or Sec23IP blocks the formation of tubular ERGIC, an unconventional cargo carrier that expedites ER-to-Golgi transport. In addition, depletion of VPS13B or Sec23IP delays ER export of procollagen, suggesting a link between procollagen secretion and joint laxity in patients with Cohen disease. Together, our study reveals a crucial role of VPS13B-Sec23IP interaction at the ERES-Golgi interface in the pathogenesis of Cohen syndrome.

VPS13B/COH1是科恩综合征(Cohen Syndrome)唯一已知的致病因子,科恩综合征是一种早发常染色体隐性发育障碍性疾病,以智力低下、发育迟缓、关节活动过度、近视和面部畸形为共同特征,但VPS13B/COH1在发病机制中的分子基础在很大程度上仍不清楚。在这里,我们发现ER出口位点(ERES)的Sec23相互作用蛋白(Sec23IP)是VPS13B的适配体,它能将VPS13B招募到ERES-高尔基界面。VPS13B通过VPS13适配体结合域(VAB)与Sec23IP直接相互作用,这种相互作用促进了ERES与高尔基体之间的结合。与疾病相关的 VPS13B-VAB 错义突变会损害与 Sec23IP 的相互作用。敲除 VPS13B 或 Sec23IP 会阻止管状 ERGIC 的形成,ERGIC 是一种非常规的货物运输载体,能加快 ER 到高尔基体的运输。此外,VPS13B或Sec23IP的缺失会延迟ER输出胶原蛋白,这表明胶原蛋白的分泌与科恩病患者关节松弛之间存在联系。总之,我们的研究揭示了 VPS13B-Sec23IP 在 ERES-Golgi 界面的相互作用在科恩综合征发病机制中的关键作用。
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引用次数: 0
Surface tension-driven sorting of human perilipins on lipid droplets. 由表面张力驱动的脂滴上人类周皮素的分选。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-09-19 DOI: 10.1083/jcb.202403064
Ana Rita Dias Araújo, Abdoul Akim Bello, Joëlle Bigay, Céline Franckhauser, Romain Gautier, Julie Cazareth, Dávid Kovács, Frédéric Brau, Nicolas Fuggetta, Alenka Čopič, Bruno Antonny

Perilipins (PLINs), the most abundant proteins on lipid droplets (LDs), display similar domain organization including amphipathic helices (AH). However, the five human PLINs bind different LDs, suggesting different modes of interaction. We established a minimal system whereby artificial LDs covered with defined polar lipids were transiently deformed to promote surface tension. Binding of purified PLIN3 and PLIN4 AH was strongly facilitated by tension but was poorly sensitive to phospholipid composition and to the presence of diacylglycerol. Accordingly, LD coverage by PLIN3 increased as phospholipid coverage decreased. In contrast, PLIN1 bound readily to LDs fully covered by phospholipids; PLIN2 showed an intermediate behavior between PLIN1 and PLIN3. In human adipocytes, PLIN3/4 were found in a soluble pool and relocated to LDs upon stimulation of fast triglyceride synthesis, whereas PLIN1 and PLIN2 localized to pre-existing LDs, consistent with the large difference in LD avidity observed in vitro. We conclude that the PLIN repertoire is adapted to handling LDs with different surface properties.

长链蛋白(PLINs)是脂滴(LDs)上最丰富的蛋白质,显示出相似的结构域组织,包括两性螺旋(AH)。然而,人类的五种磷脂蛋白与不同的脂滴结合,这表明它们之间存在不同的相互作用模式。我们建立了一个最低限度的系统,使覆盖有确定极性脂质的人工LD瞬时变形,以促进表面张力。纯化的 PLIN3 和 PLIN4 AH 的结合受到张力的强烈促进,但对磷脂成分和二酰甘油的存在却不太敏感。因此,PLIN3 的 LD 覆盖率随着磷脂覆盖率的降低而增加。相比之下,PLIN1很容易与完全被磷脂覆盖的LD结合;PLIN2的表现介于PLIN1和PLIN3之间。在人脂肪细胞中,PLIN3/4 存在于可溶性池中,并在刺激甘油三酯快速合成时迁移到低密度区,而 PLIN1 和 PLIN2 则定位到预先存在的低密度区,这与体外观察到的低密度区热敏性的巨大差异是一致的。我们得出的结论是,PLIN 基因库能够处理具有不同表面特性的 LDs。
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引用次数: 0
Detailing organelle division and segregation in Plasmodium falciparum. 详述恶性疟原虫细胞器的分裂和分离。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-11-01 DOI: 10.1083/jcb.202406064
Julie M J Verhoef, Cas Boshoven, Felix Evers, Laura J Akkerman, Barend C A Gijsbrechts, Marga van de Vegte-Bolmer, Geert-Jan van Gemert, Akhil B Vaidya, Taco W A Kooij

The malaria-causing parasite, P. falciparum, replicates through schizogony, a tightly orchestrated process where numerous daughter parasites are formed simultaneously. Proper division and segregation of one-per-cell organelles, like the mitochondrion and apicoplast, are essential, yet remain poorly understood. We developed a new reporter parasite line that allows visualization of the mitochondrion in blood and mosquito stages. Using high-resolution 3D imaging, we found that the mitochondrion orients in a cartwheel structure, prior to stepwise, non-geometric division during last-stage schizogony. Analysis of focused ion beam scanning electron microscopy data confirmed these mitochondrial division stages. Furthermore, these data allowed us to elucidate apicoplast division steps, highlighted its close association with the mitochondrion, and showed putative roles of the centriolar plaques in apicoplast segregation. These observations form the foundation for a new detailed mechanistic model of mitochondrial and apicoplast division and segregation during P. falciparum schizogony and pave the way for future studies into the proteins and protein complexes involved in organelle division and segregation.

恶性疟原虫通过分裂进行复制,这是一个紧密协调的过程,在这个过程中会同时形成许多子寄生虫。单细胞细胞器(如线粒体和细胞质)的适当分裂和分离至关重要,但人们对它们的了解仍然很少。我们开发了一种新的报告寄生虫品系,可以观察血液和蚊子阶段的线粒体。通过使用高分辨率三维成像技术,我们发现线粒体在最后阶段分裂期进行非几何级数的逐步分裂之前,是以车轮结构定向的。聚焦离子束扫描电子显微镜数据分析证实了这些线粒体分裂阶段。此外,这些数据使我们能够阐明细胞质的分裂步骤,强调其与线粒体的密切联系,并显示了中心粒斑块在细胞质分离中的潜在作用。这些观察结果为建立恶性疟原虫分裂过程中线粒体和 apicoplast 分裂和分离的新的详细机理模型奠定了基础,并为今后研究参与细胞器分裂和分离的蛋白质和蛋白质复合物铺平了道路。
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引用次数: 0
Tip60-mediated Rheb acetylation links palmitic acid with mTORC1 activation and insulin resistance. Tip60 介导的 Rheb 乙酰化将棕榈酸与 mTORC1 激活和胰岛素抵抗联系起来。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-10-18 DOI: 10.1083/jcb.202309090
Zengqi Zhao, Qiang Chen, Xiaojun Xiang, Weiwei Dai, Wei Fang, Kun Cui, Baolin Li, Qiangde Liu, Yongtao Liu, Yanan Shen, Yueru Li, Wei Xu, Kangsen Mai, Qinghui Ai

Excess dietary intake of saturated fatty acids (SFAs) induces glucose intolerance and metabolic disorders. In contrast, unsaturated fatty acids (UFAs) elicit beneficial effects on insulin sensitivity. However, it remains elusive how SFAs and UFAs signal differentially toward insulin signaling to influence glucose homeostasis. Here, using a croaker model, we report that dietary palmitic acid (PA), but not oleic acid or linoleic acid, leads to dysregulation of mTORC1, which provokes systemic insulin resistance. Mechanistically, we show that PA profoundly elevates acetyl-CoA derived from mitochondrial fatty acid β oxidation to intensify Tip60-mediated Rheb acetylation, which triggers mTORC1 activation by promoting the interaction between Rheb and FKBPs. Subsequently, hyperactivation of mTORC1 enhances IRS1 serine phosphorylation and inhibits TFEB-mediated IRS1 transcription, inducing impairment of insulin signaling. Collectively, our results reveal a conserved molecular insight into the mechanism by which Tip60-mediated Rheb acetylation induces mTORC1 activation and insulin resistance under the PA condition, which may provide therapeutic avenues to intervene in the development of T2D.

从膳食中摄入过量的饱和脂肪酸(SFA)会诱发葡萄糖不耐受症和代谢紊乱。相比之下,不饱和脂肪酸(UFAs)则对胰岛素敏感性产生有益影响。然而,SFAs 和 UFAs 如何通过不同的胰岛素信号来影响葡萄糖稳态仍是一个未知数。在这里,我们利用大黄鱼模型报告了膳食棕榈酸(PA)而非油酸或亚油酸会导致 mTORC1 失调,从而引发全身性胰岛素抵抗。从机理上讲,我们发现 PA 能显著提高线粒体脂肪酸 β 氧化产生的乙酰-CoA,从而加强 Tip60 介导的 Rheb 乙酰化,通过促进 Rheb 和 FKBPs 之间的相互作用引发 mTORC1 激活。随后,mTORC1 的过度激活会增强 IRS1 丝氨酸磷酸化并抑制 TFEB 介导的 IRS1 转录,从而导致胰岛素信号转导受损。总之,我们的研究结果揭示了Tip60介导的Rheb乙酰化在PA条件下诱导mTORC1活化和胰岛素抵抗的保守分子机制,这可能为干预T2D的发展提供了治疗途径。
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引用次数: 0
Organization of a cytoskeletal superstructure in the apical domain of intestinal tuft cells. 肠绒毛细胞顶端结构中的细胞骨架上层结构组织
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-10-01 DOI: 10.1083/jcb.202404070
Jennifer B Silverman, Evan E Krystofiak, Leah R Caplan, Ken S Lau, Matthew J Tyska

Tuft cells are a rare epithelial cell type that play important roles in sensing and responding to luminal antigens. A defining morphological feature of this lineage is the actin-rich apical "tuft," which contains large fingerlike protrusions. However, details of the cytoskeletal ultrastructure underpinning the tuft, the molecules involved in building this structure, or how it supports tuft cell biology remain unclear. In the context of the small intestine, we found that tuft cell protrusions are supported by long-core bundles that consist of F-actin crosslinked in a parallel and polarized configuration; they also contain a tuft cell-specific complement of actin-binding proteins that exhibit regionalized localization along the bundle axis. Remarkably, in the sub-apical cytoplasm, the array of core actin bundles interdigitates and co-aligns with a highly ordered network of microtubules. The resulting cytoskeletal superstructure is well positioned to support subcellular transport and, in turn, the dynamic sensing functions of the tuft cell that are critical for intestinal homeostasis.

簇细胞是一种罕见的上皮细胞类型,在感知和响应管腔抗原方面发挥着重要作用。这种细胞系的一个显著形态特征是顶端富含肌动蛋白的 "丛",其中包含大的指状突起。然而,支撑顶端突起的细胞骨架超微结构、参与构建这一结构的分子或其如何支持顶端突起细胞生物学的细节仍不清楚。在小肠的背景下,我们发现丛细胞突起由长轴束支撑,长轴束由以平行和极化构型交联的 F-肌动蛋白组成;它们还包含丛细胞特异性肌动蛋白结合蛋白补体,这些蛋白沿束轴呈现区域化定位。值得注意的是,在顶端以下的细胞质中,核心肌动蛋白束阵列与高度有序的微管网络相互咬合并共同排列。由此形成的细胞骨架上层结构能够很好地支持亚细胞运输,进而支持对肠道平衡至关重要的丛细胞动态传感功能。
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引用次数: 0
Migratory autolysosome disposal mitigates lysosome damage. 迁移性自溶体处理减轻了溶酶体损伤。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-12-02 Epub Date: 2024-09-30 DOI: 10.1083/jcb.202403195
Takami Sho, Ying Li, Haifeng Jiao, Li Yu

Lysosomes, essential for intracellular degradation and recycling, employ damage-control strategies such as lysophagy and membrane repair mechanisms to maintain functionality and cellular homeostasis. Our study unveils migratory autolysosome disposal (MAD), a response to lysosomal damage where cells expel LAMP1-LC3 positive structures via autolysosome exocytosis, requiring autophagy machinery, SNARE proteins, and cell migration. This mechanism, crucial for mitigating lysosomal damage, underscores the role of cell migration in lysosome damage control and facilitates the release of small extracellular vesicles, highlighting the intricate relationship between cell migration, organelle quality control, and extracellular vesicle release.

溶酶体是细胞内降解和再循环的关键,它采用溶酶吞噬和膜修复机制等损伤控制策略来维持功能和细胞稳态。我们的研究揭示了迁移性自溶体处理(MAD),这是一种对溶酶体损伤的反应,细胞通过自溶体外排排出 LAMP1-LC3 阳性结构,需要自噬机制、SNARE 蛋白和细胞迁移。这一机制对减轻溶酶体损伤至关重要,它强调了细胞迁移在溶酶体损伤控制中的作用,并促进了细胞外小囊泡的释放,凸显了细胞迁移、细胞器质量控制和细胞外小囊泡释放之间错综复杂的关系。
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引用次数: 0
Mitochondrial-derived compartments are multilamellar domains that encase membrane cargo and cytosol. 线粒体源性区室是一个多纤层结构域,可容纳膜货物和细胞膜。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-04 Epub Date: 2024-08-13 DOI: 10.1083/jcb.202307035
Zachary N Wilson, Matt West, Alyssa M English, Greg Odorizzi, Adam L Hughes

Preserving the health of the mitochondrial network is critical to cell viability and longevity. To do so, mitochondria employ several membrane remodeling mechanisms, including the formation of mitochondrial-derived vesicles (MDVs) and compartments (MDCs) to selectively remove portions of the organelle. In contrast to well-characterized MDVs, the distinguishing features of MDC formation and composition remain unclear. Here, we used electron tomography to observe that MDCs form as large, multilamellar domains that generate concentric spherical compartments emerging from mitochondrial tubules at ER-mitochondria contact sites. Time-lapse fluorescence microscopy of MDC biogenesis revealed that mitochondrial membrane extensions repeatedly elongate, coalesce, and invaginate to form these compartments that encase multiple layers of membrane. As such, MDCs strongly sequester portions of the outer mitochondrial membrane, securing membrane cargo into a protected domain, while also enclosing cytosolic material within the MDC lumen. Collectively, our results provide a model for MDC formation and describe key features that distinguish MDCs from other previously identified mitochondrial structures and cargo-sorting domains.

保持线粒体网络的健康对细胞的活力和寿命至关重要。为此,线粒体采用了多种膜重塑机制,包括形成线粒体衍生囊泡 (MDV) 和区室 (MDC),以选择性地移除细胞器的一部分。与表征明确的 MDVs 不同,MDCs 形成和组成的显著特征仍不清楚。在这里,我们利用电子断层扫描技术观察到,MDCs 以大型多纤毛结构域的形式形成,在 ER 线粒体与线粒体的接触部位产生从线粒体小管出现的同心球形隔室。对 MDC 生物发生过程的延时荧光显微镜观察发现,线粒体膜延伸部分反复伸长、凝聚和内陷,形成了这些包裹多层膜的区室。因此,MDCs 能强力封闭线粒体外膜的一部分,将膜货物固定在一个受保护的区域内,同时也将细胞质封闭在 MDC 内腔中。总之,我们的研究结果为 MDC 的形成提供了一个模型,并描述了将 MDC 与之前发现的其他线粒体结构和货物分类域区分开来的关键特征。
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引用次数: 0
A complex of the lipid transport ER proteins TMEM24 and C2CD2 with band 4.1 at cell-cell contacts. 脂质转运 ER 蛋白 TMEM24 和 C2CD2 与带 4.1 在细胞-细胞接触处的复合物。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-04 Epub Date: 2024-08-19 DOI: 10.1083/jcb.202311137
Ben Johnson, Maria Iuliano, TuKiet T Lam, Thomas Biederer, Pietro V De Camilli

Junctions between the ER and plasma membrane (PM) are implicated in calcium homeostasis, non-vesicular lipid transfer, and other cellular functions. Two ER proteins that function both as tethers to the PM via a polybasic C-terminus motif and as phospholipid transporters are brain-enriched TMEM24 (C2CD2L) and its paralog C2CD2. We report that both proteins also form a complex with band 4.1 family members, which in turn bind PM proteins including cell adhesion molecules such as SynCAM 1. This complex enriches TMEM24 and C2CD2 containing ER/PM junctions at sites of cell contacts. Dynamic properties of TMEM24-dependent ER/PM junctions are impacted when band 4.1 is part of the junction, as TMEM24 at cell-adjacent ER/PM junctions is not shed from the PM by calcium rise, unlike TMEM24 at non-cell adjacent junctions. Lipid transport between the ER and the PM by TMEM24 and C2CD2 at sites where cells, including neurons, contact other cells may participate in adaptive responses to cell contact-dependent signaling.

ER和质膜(PM)之间的连接与钙平衡、非囊泡脂质转移和其他细胞功能有关。脑富集的 TMEM24(C2CD2L)及其同源物 C2CD2 是两种既能通过多基态 C 端基团与质膜连接又能作为磷脂转运体的 ER 蛋白。我们报告说,这两种蛋白还与带状 4.1 家族成员形成复合物,而带状 4.1 家族成员又与包括细胞粘附分子(如 SynCAM 1)在内的 PM 蛋白结合。这种复合物在细胞接触部位富集了含有 ER/PM 连接的 TMEM24 和 C2CD2。当带 4.1 成为连接点的一部分时,依赖 TMEM24 的 ER/PM 连接点的动态特性会受到影响,因为细胞相邻 ER/PM 连接点上的 TMEM24 不会因钙升高而从 PM 上脱落,这与非细胞相邻连接点上的 TMEM24 不同。在细胞(包括神经元)与其他细胞接触的部位,TMEM24 和 C2CD2 在 ER 和 PM 之间的脂质运输可能参与了对细胞接触依赖性信号的适应性反应。
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引用次数: 0
Cyclin B3 is a dominant fast-acting cyclin that drives rapid early embryonic mitoses. 细胞周期蛋白 B3 是一种显性快速作用细胞周期蛋白,它能驱动早期胚胎的快速有丝分裂。
IF 7.4 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-11-04 Epub Date: 2024-08-06 DOI: 10.1083/jcb.202308034
Pablo Lara-Gonzalez, Smriti Variyar, Shabnam Moghareh, Anh Cao Ngoc Nguyen, Amrutha Kizhedathu, Jacqueline Budrewicz, Aleesa Schlientz, Neha Varshney, Andrew Bellaart, Karen Oegema, Lee Bardwell, Arshad Desai

Mitosis in early embryos often proceeds at a rapid pace, but how this pace is achieved is not understood. Here, we show that cyclin B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo. Cyclins B1 and B2 support slow mitosis (NEBD to anaphase ∼600 s), but the presence of cyclin B3 dominantly drives the approximately threefold faster mitosis observed in wildtype. Multiple mitotic events are slowed down in cyclin B1 and B2-driven mitosis, and cyclin B3-associated Cdk1 H1 kinase activity is ∼25-fold more active than cyclin B1-associated Cdk1. Addition of cyclin B1 to fast cyclin B3-only mitosis introduces an ∼60-s delay between completion of chromosome alignment and anaphase onset; this delay, which is important for segregation fidelity, is dependent on inhibitory phosphorylation of the anaphase activator Cdc20. Thus, cyclin B3 dominance, coupled to a cyclin B1-dependent delay that acts via Cdc20 phosphorylation, sets the rapid pace and ensures mitotic fidelity in the early C. elegans embryo.

早期胚胎的有丝分裂通常以很快的速度进行,但这种速度是如何实现的尚不清楚。在这里,我们发现细胞周期蛋白 B3 是优雅小鼠胚胎快速有丝分裂的主要驱动力。细胞周期蛋白 B1 和 B2 支持缓慢的有丝分裂(从 NEBD 到无丝分裂 ∼600 秒),但细胞周期蛋白 B3 的存在主导性地推动了野生型中观察到的约三倍快的有丝分裂。在细胞周期蛋白 B1 和 B2 驱动的有丝分裂过程中,多个有丝分裂事件被减慢,细胞周期蛋白 B3 相关的 Cdk1 H1 激酶活性比细胞周期蛋白 B1 相关的 Cdk1 活性高 25 倍。在仅有细胞周期蛋白 B3 的快速有丝分裂中加入细胞周期蛋白 B1,会在染色体排列完成和无丝分裂开始之间产生 60 秒的延迟;这种延迟对分离的保真度非常重要,它依赖于无丝分裂激活剂 Cdc20 的抑制性磷酸化。因此,细胞周期蛋白 B3 的优势加上细胞周期蛋白 B1 依赖性延迟(通过 Cdc20 磷酸化起作用),为早期秀丽隐杆线虫胚胎的有丝分裂设定了快节奏,并确保了有丝分裂的保真度。
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引用次数: 0
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