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Sulfur incorporation into biomolecules: recent advances. 硫与生物分子的结合:最新进展。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-01 Epub Date: 2022-11-20 DOI: 10.1080/10409238.2022.2141678
Shramana Chatterjee, Robert P Hausinger

Sulfur is an essential element for a variety of cellular constituents in all living organisms and adds considerable functionality to a wide range of biomolecules. The pathways for incorporating sulfur into central metabolites of the cell such as cysteine, methionine, cystathionine, and homocysteine have long been established. Furthermore, the importance of persulfide intermediates during the biosynthesis of thionucleotide-containing tRNAs, iron-sulfur clusters, thiamin diphosphate, and the molybdenum cofactor are well known. This review briefly surveys these topics while emphasizing more recent aspects of sulfur metabolism that involve unconventional biosynthetic pathways. Sacrificial sulfur transfers from protein cysteinyl side chains to precursors of thiamin and the nickel-pincer nucleotide (NPN) cofactor are described. Newer aspects of synthesis for lipoic acid, biotin, and other compounds are summarized, focusing on the requisite iron-sulfur cluster destruction. Sulfur transfers by using a noncore sulfide ligand bound to a [4Fe-4S] cluster are highlighted for generating certain thioamides and for alternative biosynthetic pathways of thionucleotides and the NPN cofactor. Thioamide formation by activating an amide oxygen atom via phosphorylation also is illustrated. The discussion of these topics stresses the chemical reaction mechanisms of the transformations and generally avoids comments on the gene/protein nomenclature or the sources of the enzymes. This work sets the stage for future efforts to decipher the diverse mechanisms of sulfur incorporation into biological molecules.

硫是所有生物体中各种细胞成分的必需元素,并为广泛的生物分子增加了相当大的功能。将硫纳入细胞中心代谢物(如半胱氨酸、蛋氨酸、半胱甘氨酸和同型半胱氨酸)的途径早已确立。此外,过硫中间体在含硫核苷酸的trna、铁硫簇、硫胺二磷酸和钼辅助因子的生物合成中的重要性是众所周知的。本文简要综述了这些主题,同时强调了涉及非常规生物合成途径的硫代谢的最新方面。牺牲硫从蛋白质半胱氨酸侧链转移到硫胺素和镍钳核苷酸(NPN)辅因子的前体。综述了硫辛酸、生物素和其他化合物合成的最新进展,重点介绍了铁硫团簇破坏的必要条件。利用与[4Fe-4S]簇结合的非核硫化物配体进行硫转移,可以生成某些硫酰胺,也可以替代硫核苷酸和NPN辅因子的生物合成途径。还说明了通过磷酸化激活酰胺氧原子形成硫酰胺。这些主题的讨论强调转化的化学反应机制,一般避免评论基因/蛋白质的命名法或酶的来源。这项工作为未来破译硫与生物分子结合的不同机制奠定了基础。
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引用次数: 2
Milk glycan metabolism by intestinal bifidobacteria: insights from comparative genomics. 肠道双歧杆菌的牛奶糖代谢:比较基因组学的启示。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-01 Epub Date: 2023-03-03 DOI: 10.1080/10409238.2023.2182272
Aleksandr A Arzamasov, Andrei L Osterman

Bifidobacteria are early colonizers of the human neonatal gut and provide multiple health benefits to the infant, including inhibiting the growth of enteropathogens and modulating the immune system. Certain Bifidobacterium species prevail in the gut of breastfed infants due to the ability of these microorganisms to selectively forage glycans present in human milk, specifically human milk oligosaccharides (HMOs) and N-linked glycans. Therefore, these carbohydrates serve as promising prebiotic dietary supplements to stimulate the growth of bifidobacteria in the guts of children suffering from impaired gut microbiota development. However, the rational formulation of milk glycan-based prebiotics requires a detailed understanding of how bifidobacteria metabolize these carbohydrates. Accumulating biochemical and genomic data suggest that HMO and N-glycan assimilation abilities vary remarkably within the Bifidobacterium genus, both at the species and strain levels. This review focuses on the delineation and genome-based comparative analysis of differences in respective biochemical pathways, transport systems, and associated transcriptional regulatory networks, providing a foundation for genomics-based projection of milk glycan utilization capabilities across a rapidly growing number of sequenced bifidobacterial genomes and metagenomic datasets. This analysis also highlights remaining knowledge gaps and suggests directions for future studies to optimize the formulation of milk-glycan-based prebiotics that target bifidobacteria.

双歧杆菌是人类新生儿肠道的早期定植菌,对婴儿的健康有多种益处,包括抑制肠道病原体的生长和调节免疫系统。母乳喂养的婴儿肠道中普遍存在某些双歧杆菌物种,这是因为这些微生物能够选择性地觅食母乳中的糖类,特别是母乳低聚糖(HMO)和N-连接糖。因此,这些碳水化合物是很有前景的益生元膳食补充剂,可刺激肠道微生物群发育受损儿童肠道中双歧杆菌的生长。然而,要合理配制基于牛奶聚糖的益生元,就必须详细了解双歧杆菌是如何代谢这些碳水化合物的。不断积累的生化和基因组数据表明,双歧杆菌属内的 HMO 和 N-糖同化能力在物种和菌株水平上都存在显著差异。本综述侧重于对各自生化途径、转运系统和相关转录调控网络的差异进行划分和基于基因组的比较分析,为基于基因组学的牛奶糖利用能力预测提供基础,这些预测涉及快速增长的双歧杆菌基因组测序和元基因组数据集。这项分析还强调了尚存在的知识空白,并为今后优化以双歧杆菌为目标的牛奶糖基益生元配方的研究提出了方向。
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引用次数: 0
G-quadruplexes in bacteria: insights into the regulatory roles and interacting proteins of non-canonical nucleic acid structures. 细菌中的G-四链体:对非规范核酸结构的调节作用和相互作用蛋白的见解。
IF 6.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-01 Epub Date: 2023-03-31 DOI: 10.1080/10409238.2023.2181310
Rachel R Cueny, Sarah D McMillan, James L Keck

G-quadruplexes (G4s) are highly stable, non-canonical DNA or RNA structures that can form in guanine-rich stretches of nucleic acids. G4-forming sequences have been found in all domains of life, and proteins that bind and/or resolve G4s have been discovered in both bacterial and eukaryotic organisms. G4s regulate a variety of cellular processes through inhibitory or stimulatory roles that depend upon their positions within genomes or transcripts. These include potential roles as impediments to genome replication, transcription, and translation or, in other contexts, as activators of genome stability, transcription, and recombination. This duality suggests that G4 sequences can aid cellular processes but that their presence can also be problematic. Despite their documented importance in bacterial species, G4s remain understudied in bacteria relative to eukaryotes. In this review, we highlight the roles of bacterial G4s by discussing their prevalence in bacterial genomes, the proteins that bind and unwind G4s in bacteria, and the processes regulated by bacterial G4s. We identify limitations in our current understanding of the functions of G4s in bacteria and describe new avenues for studying these remarkable nucleic acid structures.

G-四链体(G4s)是高度稳定的非经典DNA或RNA结构,可以在富含鸟嘌呤的核酸片段中形成。在生命的所有领域都发现了G4形成序列,在细菌和真核生物中都发现了结合和/或解析G4s的蛋白质。G4s通过抑制或刺激作用调节各种细胞过程,这取决于它们在基因组或转录物中的位置。这些包括作为基因组复制、转录和翻译的障碍的潜在作用,或者在其他情况下,作为基因组稳定性、转录和重组的激活剂。这种双重性表明G4序列可以帮助细胞过程,但它们的存在也可能是有问题的。尽管G4s在细菌物种中具有重要意义,但相对于真核生物,G4s在菌株中的研究仍然不足。在这篇综述中,我们通过讨论细菌G4s在细菌基因组中的普遍性、细菌中结合和释放G4s的蛋白质以及细菌G4s调节的过程来强调细菌G4s的作用。我们确定了目前对G4s在细菌中的功能理解的局限性,并描述了研究这些显著核酸结构的新途径。
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引用次数: 0
Overview of physiological, biochemical, and regulatory aspects of nitrogen fixation in Azotobacter vinelandii. 黄氏固氮固氮的生理、生化和调控方面综述。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-01 DOI: 10.1080/10409238.2023.2181309
Julia S Martin Del Campo, Jack Rigsbee, Marcelo Bueno Batista, Florence Mus, Luis M Rubio, Oliver Einsle, John W Peters, Ray Dixon, Dennis R Dean, Patricia C Dos Santos

Understanding how Nature accomplishes the reduction of inert nitrogen gas to form metabolically tractable ammonia at ambient temperature and pressure has challenged scientists for more than a century. Such an understanding is a key aspect toward accomplishing the transfer of the genetic determinants of biological nitrogen fixation to crop plants as well as for the development of improved synthetic catalysts based on the biological mechanism. Over the past 30 years, the free-living nitrogen-fixing bacterium Azotobacter vinelandii emerged as a preferred model organism for mechanistic, structural, genetic, and physiological studies aimed at understanding biological nitrogen fixation. This review provides a contemporary overview of these studies and places them within the context of their historical development.

一个多世纪以来,了解大自然如何在环境温度和压力下完成惰性氮气的还原,形成可代谢的氨,一直是科学家们面临的挑战。这样的理解是实现生物固氮遗传决定因素向作物植物转移以及基于生物机制开发改进的合成催化剂的关键方面。在过去的30年里,自由生活的固氮细菌Azotobacter vinelandii成为了解生物固氮机制、结构、遗传和生理研究的首选模式生物。这篇综述提供了这些研究的当代概况,并将它们置于其历史发展的背景下。
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引用次数: 5
2-5A-Mediated decay (2-5AMD): from antiviral defense to control of host RNA. 2-5A介导的衰变(2-5AMD):从抗病毒防御到控制宿主RNA。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-01 Epub Date: 2023-03-20 DOI: 10.1080/10409238.2023.2181308
Eliza Prangley, Alexei Korennykh

Mammalian cells are exquisitely sensitive to the presence of double-stranded RNA (dsRNA), a molecule that they interpret as a signal of viral presence requiring immediate attention. Upon sensing dsRNA cells activate the innate immune response, which involves transcriptional mechanisms driving inflammation and secretion of interferons (IFNs) and interferon-stimulated genes (ISGs), as well as synthesis of RNA-like signaling molecules comprised of three or more 2'-5'-linked adenylates (2-5As). 2-5As were discovered some forty years ago and described as IFN-induced inhibitors of protein synthesis. The efforts of many laboratories, aimed at elucidating the molecular mechanism and function of these mysterious RNA-like signaling oligonucleotides, revealed that 2-5A is a specific ligand for the kinase-family endonuclease RNase L. RNase L decays single-stranded RNA (ssRNA) from viruses and mRNAs (as well as other RNAs) from hosts in a process we proposed to call 2-5A-mediated decay (2-5AMD). During recent years it has become increasingly recognized that 2-5AMD is more than a blunt tool of viral RNA destruction, but a pathway deeply integrated into sensing and regulation of endogenous RNAs. Here we present an overview of recently emerged roles of 2-5AMD in host RNA regulation.

哺乳动物细胞对双链RNA(dsRNA)的存在非常敏感,他们将这种分子解释为病毒存在的信号,需要立即关注。在感应到dsRNA细胞后,激活先天免疫反应,这涉及驱动炎症和干扰素(IFN)和干扰素刺激基因(ISG)分泌的转录机制,以及由三种或多种2'-5'-连接的腺苷酸(2-5As)组成的RNA样信号分子的合成。2-5As是大约四十年前发现的,被描述为IFN诱导的蛋白质合成抑制剂。许多实验室致力于阐明这些神秘的类RNA信号寡核苷酸的分子机制和功能,结果表明2-5A是激酶家族核酸内切酶RNase L的特异性配体。RNase L在我们提出称为2-5A介导的衰变(2-5AMD)的过程中衰变来自病毒的单链RNA(ssRNA)和来自宿主的mRNA(以及其他RNA)。近年来,人们越来越认识到2-5AMD不仅仅是一种破坏病毒RNA的钝工具,而是一种深入整合到内源性RNA传感和调节中的途径。在这里,我们概述了最近出现的2-5AMD在宿主RNA调节中的作用。
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引用次数: 0
Reversible and bidirectional signaling of notch ligands. 缺口配体的可逆和双向信号传导。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-08-01 DOI: 10.1080/10409238.2022.2113029
Elenaé Vázquez-Ulloa, Kai-Lan Lin, Marcela Lizano, Cecilia Sahlgren

The Notch signaling pathway is a direct cell-cell communication system involved in a wide variety of biological processes, and its disruption is observed in several pathologies. The pathway is comprised of a ligand-expressing (sender) cell and a receptor-expressing (receiver) cell. The canonical ligands are members of the Delta/Serrate/Lag-1 (DSL) family of proteins. Their binding to a Notch receptor in a neighboring cell induces a conformational change in the receptor, which will undergo regulated intramembrane proteolysis (RIP), liberating the Notch intracellular domain (NICD). The NICD is translocated to the nucleus and promotes gene transcription. It has been demonstrated that the ligands can also undergo RIP and nuclear translocation, suggesting a function for the ligands in the sender cell and possible bidirectionality of the Notch pathway. Although the complete mechanism of ligand processing is not entirely understood, and its dependence on Notch receptors has not been ruled out. Also, ligands have autonomous functions beyond Notch activation. Here we review the concepts of reverse and bidirectional signalization of DSL proteins and discuss the characteristics that make them more than just ligands of the Notch pathway.

Notch信号通路是一个直接的细胞-细胞通讯系统,参与多种生物过程,在多种病理中观察到它的破坏。该途径由表达配体的细胞(发送者)和表达受体的细胞(接收者)组成。规范配体是Delta/Serrate/Lag-1 (DSL)蛋白家族的成员。它们与邻近细胞中的Notch受体结合,诱导受体发生构象变化,从而发生受调控的膜内蛋白水解(RIP),释放Notch胞内结构域(NICD)。NICD易位到细胞核并促进基因转录。研究表明,这些配体也可以经历RIP和核易位,这表明配体在发送细胞中起作用,并且可能是Notch通路的双向性。虽然配体加工的完整机制尚不完全清楚,但它对Notch受体的依赖性也不排除。此外,配体具有Notch激活之外的自主功能。在这里,我们回顾了DSL蛋白的反向和双向信号的概念,并讨论了使它们不仅仅是Notch途径的配体的特征。
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引用次数: 1
Creation and resolution of non-B-DNA structural impediments during replication. 在复制过程中产生并解决非 B-DNA 结构障碍。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-08-01 Epub Date: 2022-09-28 DOI: 10.1080/10409238.2022.2121803
Christopher Mellor, Consuelo Perez, Julian E Sale

During replication, folding of the DNA template into non-B-form secondary structures provides one of the most abundant impediments to the smooth progression of the replisome. The core replisome collaborates with multiple accessory factors to ensure timely and accurate duplication of the genome and epigenome. Here, we discuss the forces that drive non-B structure formation and the evidence that secondary structures are a significant and frequent source of replication stress that must be actively countered. Taking advantage of recent advances in the molecular and structural biology of the yeast and human replisomes, we examine how structures form and how they may be sensed and resolved during replication.

在复制过程中,DNA 模板折叠成非 B 型二级结构是阻碍复制体顺利进行的最大障碍之一。核心复制体与多种辅助因子协作,确保及时准确地复制基因组和表观基因组。在这里,我们将讨论驱动非 B 结构形成的力量,以及二级结构是必须积极应对的重要且频繁的复制压力来源的证据。利用酵母和人类复制体分子和结构生物学的最新进展,我们研究了结构是如何形成的,以及在复制过程中如何感知和解决这些结构。
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引用次数: 0
What makes functional amyloids work? 是什么使功能性淀粉样蛋白起作用?
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-08-01 DOI: 10.1080/10409238.2022.2113030
Ansgar B Siemer

Although first described in the context of disease, cross-β (amyloid) fibrils have also been found as functional entities in all kingdoms of life. However, what are the specific properties of the cross-β fibril motif that convey biological function, make them especially suited for their particular purpose, and distinguish them from other fibrils found in biology? This review approaches these questions by arguing that cross-β fibrils are highly periodic, stable, and self-templating structures whose formation is accompanied by substantial conformational change that leads to a multimerization of their core and framing sequences. A discussion of each of these properties is followed by selected examples of functional cross-β fibrils that show how function is usually achieved by leveraging many of these properties.

虽然最初是在疾病的背景下被描述的,但交叉β(淀粉样蛋白)原纤维也被发现是所有生命领域的功能实体。然而,交叉β原纤维基序传达生物学功能的具体特性是什么,使它们特别适合于它们的特定用途,并将它们与生物学中发现的其他原纤维区分开来?这篇综述通过论证交叉β原纤维是高度周期性的、稳定的和自模板的结构,其形成伴随着大量的构象变化,导致其核心和框架序列的多聚合。对这些特性的讨论之后,选择功能性交叉β原纤维的例子,展示了通常如何通过利用许多这些特性来实现功能。
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引用次数: 2
Hypoxia-regulated microRNAs: the molecular drivers of tumor progression. 低氧调控的microrna:肿瘤进展的分子驱动因素。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-08-01 DOI: 10.1080/10409238.2022.2088684
Sakunie Sawai, Pooi-Fong Wong, Thamil Selvee Ramasamy

Hypoxia is a common feature of the tumor microenvironment (TME) of nearly all solid tumors, leading to therapeutic failure. The changes in stiffness of the extracellular matrix (ECM), pH gradients, and chemical balance that contribute to multiple cancer hallmarks are closely regulated by intratumoral oxygen tension via its primary mediators, hypoxia-inducible factors (HIFs). HIFs, especially HIF-1α, influence these changes in the TME by regulating vital cancer-associated signaling pathways and cellular processes including MAPK/ERK, NF-κB, STAT3, PI3K/Akt, Wnt, p53, and glycolysis. Interestingly, research has revealed the involvement of epigenetic regulation by hypoxia-regulated microRNAs (HRMs) of downstream target genes involved in these signaling. Through literature search and analysis, we identified 48 HRMs that have a functional role in the regulation of 5 key cellular processes: proliferation, metabolism, survival, invasion and migration, and immunoregulation in various cancers in hypoxic condition. Among these HRMs, 17 were identified to be directly associated with HIFs which include miR-135b, miR-145, miR-155, miR-181a, miR-182, miR-210, miR-224, miR-301a, and miR-675-5p as oncomiRNAs, and miR-100-5p, miR-138, miR-138-5p, miR-153, miR-22, miR-338-3p, miR-519d-3p, and miR-548an as tumor suppressor miRNAs. These HRMs serve as a potential lead in the development of miRNA-based targeted therapy for advanced solid tumors. Future development of combined HIF-targeted and miRNA-targeted therapy is possible, which requires comprehensive profiling of HIFs-HRMs regulatory network, and improved formula of the delivery vehicles to enhance the therapeutic kinetics of the targeted cancer therapy (TCT) moving forward.

缺氧是几乎所有实体瘤肿瘤微环境(TME)的共同特征,导致治疗失败。细胞外基质(ECM)硬度、pH梯度和化学平衡的变化导致多种癌症特征,这些变化是由肿瘤内氧张力通过其主要介质缺氧诱导因子(hif)密切调节的。hif,尤其是HIF-1α,通过调节重要的癌症相关信号通路和细胞过程,包括MAPK/ERK、NF-κB、STAT3、PI3K/Akt、Wnt、p53和糖酵解,影响TME的这些变化。有趣的是,研究揭示了参与这些信号传导的下游靶基因的缺氧调节microRNAs (HRMs)参与表观遗传调控。通过文献检索和分析,我们确定了48个HRMs,它们在缺氧条件下调节各种癌症的5个关键细胞过程:增殖、代谢、生存、侵袭和迁移以及免疫调节中发挥功能作用。在这些HRMs中,有17个被确定与hif直接相关,其中miR-135b、miR-145、miR-155、miR-181a、miR-182、miR-210、miR-224、miR-301a和miR-675-5p为肿瘤mirna, miR-100-5p、miR-138、miR-138-5p、miR-153、miR-22、miR-338-3p、miR-519d-3p和miR-548an为肿瘤抑制mirna。这些HRMs在开发基于mirna的晚期实体瘤靶向治疗方面具有潜在的引领作用。未来hif靶向治疗和mirna靶向治疗的联合发展是可能的,这需要对hif - hrms调控网络进行全面分析,并改进递送载体的配方,以提高靶向癌症治疗(TCT)的治疗动力学。
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引用次数: 5
Energetics, kinetics, and pathways of SNARE assembly in membrane fusion. 膜融合中SNARE组装的能量学、动力学和途径。
IF 6.5 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-08-01 DOI: 10.1080/10409238.2022.2121804
Yongli Zhang, Lu Ma, Huan Bao

Fusion of transmitter-containing vesicles with plasma membranes at the synaptic and neuromuscular junctions mediates neurotransmission and muscle contractions, respectively, thereby underlying all thoughts and actions. The fusion process is driven by the coupled folding and assembly of three synaptic SNARE proteins--syntaxin-1 and SNAP-25 on the target plasma membrane (t-SNAREs) and VAMP2 on the vesicular membrane (v-SNARE) into a four-helix bundle. Their assembly is chaperoned by Munc18-1 and many other proteins to achieve the speed and accuracy required for neurotransmission. However, the physiological pathway of SNARE assembly and its coupling to membrane fusion remains unclear. Here, we review recent progress in understanding SNARE assembly and membrane fusion, with a focus on results obtained by single-molecule manipulation approaches and electric recordings of single fusion pores. We describe two pathways of synaptic SNARE assembly, their associated intermediates, energetics, and kinetics. Assembly of the three SNAREs in vitro begins with the formation of a t-SNARE binary complex, on which VAMP2 folds in a stepwise zipper-like fashion. Munc18-1 significantly alters the SNARE assembly pathway: syntaxin-1 and VAMP2 first bind on the surface of Munc18-1 to form a template complex, with which SNAP-25 associates to conclude SNARE assembly and displace Munc18-1. During membrane fusion, multiple trans-SNARE complexes cooperate to open a dynamic fusion pore in a manner dependent upon their copy number and zippering states. Together, these results demonstrate that stepwise and cooperative SNARE assembly drive stagewise membrane fusion.

含有递质的囊泡与突触和神经肌肉连接处的质膜的融合分别介导神经传递和肌肉收缩,从而成为所有思想和行为的基础。融合过程是由三个突触SNARE蛋白耦合折叠和组装驱动的,syntaxin-1和SNAP-25在靶质膜上(t-SNAREs)和VAMP2在泡膜上(v-SNARE)形成一个四螺旋束。它们的组装由Munc18-1和许多其他蛋白质陪同,以达到神经传递所需的速度和准确性。然而,SNARE组装的生理途径及其与膜融合的耦合尚不清楚。在这里,我们回顾了最近在了解SNARE组装和膜融合方面的进展,重点介绍了单分子操作方法和单融合孔的电记录所获得的结果。我们描述了突触SNARE组装的两种途径,它们的相关中间体,能量学和动力学。三个snare在体外的组装始于t-SNARE二元复合物的形成,VAMP2在其上以类似拉链的方式逐步折叠。Munc18-1显著改变了SNARE组装途径:syntaxin-1和VAMP2首先结合在Munc18-1表面形成模板复合物,SNAP-25与模板复合物结合完成SNARE组装并取代Munc18-1。在膜融合过程中,多个trans-SNARE复合物以依赖于其拷贝数和拉链状态的方式合作打开动态融合孔。综上所述,这些结果表明,阶梯式和协同式SNARE组装驱动了分阶段的膜融合。
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引用次数: 9
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