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A Life of Translocations. 易位的一生。
IF 12.1 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-07-02 DOI: 10.1146/annurev-biochem-030122-040444
Tom A Rapoport

Writing a career retrospective for this prestigious series is a huge challenge. Is my story really of that much interest? One thing that is different about my life in science is the heavy influence of the turmoil of the past century. Born in the US, raised in East Germany, and returning to the US relatively late in life, I experienced research under both suboptimal and privileged conditions. My scientific story, like the political winds that blew me from one continent to the next, involved shifts into different fields. For advice to young scientists, I would suggest: Don't be afraid to start something new, it pays to be persistent, and science is a passion. In addition to telling my own story, this article also provides the opportunity to express my gratitude to my trainees and colleagues and to convey my conviction that we have the best job on earth.

为这个著名的系列节目撰写职业回顾是一个巨大的挑战。我的故事真的那么有趣吗?在我的科学生涯中,有一件事是不同的,那就是上个世纪的动荡对我的影响很大。我出生在美国,在东德长大,很晚才回到美国,经历了次优和特权条件下的研究。我的科学经历,就像把我从一个大陆吹到另一个大陆的政治之风,涉及到不同领域的转变。对于年轻科学家的建议,我建议:不要害怕开始新事物,坚持不懈是值得的,科学是一种激情。除了讲述我自己的故事外,这篇文章还提供了一个机会来表达我对我的学员和同事的感激之情,并传达我的信念:我们拥有世界上最好的工作。预计《生物化学年度评论》第93卷的最终在线出版日期是2024年6月。修订后的估计数请参阅http://www.annualreviews.org/page/journal/pubdates。
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引用次数: 0
Lipid Quality Control and Ferroptosis: From Concept to Mechanism. 脂质控制与铁下垂:从概念到机制。
IF 12.1 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-07-02 DOI: 10.1146/annurev-biochem-052521-033527
Zhipeng Li, Mike Lange, Scott J Dixon, James A Olzmann

Cellular quality control systems sense and mediate homeostatic responses to prevent the buildup of aberrant macromolecules, which arise from errors during biosynthesis, damage by environmental insults, or imbalances in enzymatic and metabolic activity. Lipids are structurally diverse macromolecules that have many important cellular functions, ranging from structural roles in membranes to functions as signaling and energy-storage molecules. As with other macromolecules, lipids can be damaged (e.g., oxidized), and cells require quality control systems to ensure that nonfunctional and potentially toxic lipids do not accumulate. Ferroptosis is a form of cell death that results from the failure of lipid quality control and the consequent accumulation of oxidatively damaged phospholipids. In this review, we describe a framework for lipid quality control, using ferroptosis as an illustrative example to highlight concepts related to lipid damage, membrane remodeling, and suppression or detoxification of lipid damage via preemptive and damage-repair lipid quality control pathways.

细胞质量控制系统感知和介导稳态反应,以防止异常大分子的积累,这些异常大分子是由生物合成过程中的错误、环境损害或酶和代谢活动的不平衡引起的。脂质是结构多样的大分子,具有许多重要的细胞功能,从膜的结构作用到信号和能量储存分子。与其他大分子一样,脂质会被破坏(如氧化),细胞需要质量控制系统来确保无功能和潜在毒性的脂质不会积聚。铁死亡是一种细胞死亡形式,由脂质控制失败和氧化损伤磷脂的积累引起。在这篇综述中,我们描述了一个脂质控制的框架,以铁下沉为例,强调与脂质损伤、膜重塑以及通过先发制人和损伤修复脂质控制途径抑制或解毒脂质损伤相关的概念。预计《生物化学年度评论》第93卷的最终在线出版日期是2024年6月。修订后的估计数请参阅http://www.annualreviews.org/page/journal/pubdates。
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引用次数: 0
Structural Biochemistry of Muscle Contraction. 肌肉收缩的结构生物化学。
IF 16.6 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 DOI: 10.1146/annurev-biochem-052521-042909
Zhexin Wang, Stefan Raunser

Muscles are essential for movement and heart function. Contraction and relaxation of muscles rely on the sliding of two types of filaments-the thin filament and the thick myosin filament. The thin filament is composed mainly of filamentous actin (F-actin), tropomyosin, and troponin. Additionally, several other proteins are involved in the contraction mechanism, and their malfunction can lead to diverse muscle diseases, such as cardiomyopathies. We review recent high-resolution structural data that explain the mechanism of action of muscle proteins at an unprecedented level of molecular detail. We focus on the molecular structures of the components of the thin and thick filaments and highlight the mechanisms underlying force generation through actin-myosin interactions, as well as Ca2+-dependent regulation via the dihydropyridine receptor, the ryanodine receptor, and troponin. We particularly emphasize the impact of cryo-electron microscopy and cryo-electron tomography in leading muscle research into a new era.

肌肉对运动和心脏功能至关重要。肌肉的收缩和松弛依赖于两种纤维的滑动——细纤维和粗肌球蛋白纤维。细丝主要由丝状肌动蛋白(F-actin)、原肌球蛋白和肌钙蛋白组成。此外,其他几种蛋白质也参与收缩机制,它们的功能障碍可导致多种肌肉疾病,如心肌病。我们回顾了最近的高分辨率结构数据,这些数据在前所未有的分子细节水平上解释了肌肉蛋白的作用机制。我们专注于细纤维和粗纤维成分的分子结构,并强调通过肌动蛋白-肌球蛋白相互作用产生力的机制,以及通过二氢吡啶受体、红嘌呤受体和肌钙蛋白进行的Ca2+依赖性调节。我们特别强调低温电子显微镜和低温电子断层扫描在引领肌肉研究进入新时代的影响。
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引用次数: 3
Transcription-Coupled Nucleotide Excision Repair and the Transcriptional Response to UV-Induced DNA Damage. 转录偶联核苷酸切除修复和紫外线诱导DNA损伤的转录反应。
IF 16.6 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 DOI: 10.1146/annurev-biochem-052621-091205
Nicolás Nieto Moreno, Anouk M Olthof, Jesper Q Svejstrup

Ultraviolet (UV) irradiation and other genotoxic stresses induce bulky DNA lesions, which threaten genome stability and cell viability. Cells have evolved two main repair pathways to remove such lesions: global genome nucleotide excision repair (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER). The modes by which these subpathways recognize DNA lesions are distinct, but they converge onto the same downstream steps for DNA repair. Here, we first summarize the current understanding of these repair mechanisms, specifically focusing on the roles of stalled RNA polymerase II, Cockayne syndrome protein B (CSB), CSA and UV-stimulated scaffold protein A (UVSSA) in TC-NER. We also discuss the intriguing role of protein ubiquitylation in this process. Additionally, we highlight key aspects of the effect of UV irradiation on transcription and describe the role of signaling cascades in orchestrating this response. Finally, we describe the pathogenic mechanisms underlying xeroderma pigmentosum and Cockayne syndrome, the two main diseases linked to mutations in NER factors.

紫外线(UV)照射和其他基因毒性应激可诱导大量DNA损伤,从而威胁到基因组的稳定性和细胞的活力。细胞已经进化出两种主要的修复途径来去除这些病变:全球基因组核苷酸切除修复(GG-NER)和转录偶联核苷酸切除修复(TC-NER)。这些亚通路识别DNA损伤的模式是不同的,但它们汇聚到DNA修复的相同下游步骤。在这里,我们首先总结了目前对这些修复机制的理解,特别关注了停滞RNA聚合酶II、Cockayne综合征蛋白B (CSB)、CSA和uv刺激支架蛋白A (uvsa)在TC-NER中的作用。我们还讨论了蛋白质泛素化在这一过程中的有趣作用。此外,我们强调了紫外线照射对转录影响的关键方面,并描述了信号级联在协调这种反应中的作用。最后,我们描述了色素干皮病和Cockayne综合征的致病机制,这两种主要疾病与NER因子突变有关。
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引用次数: 6
Molecular Mechanisms of Transcription-Coupled Repair. 转录偶联修复的分子机制。
IF 16.6 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 DOI: 10.1146/annurev-biochem-041522-034232
Christopher P Selby, Laura A Lindsey-Boltz, Wentao Li, Aziz Sancar

Transcription-coupled repair (TCR), discovered as preferential nucleotide excision repair of UV-induced cyclobutane pyrimidine dimers located in transcribed mammalian genes compared to those in nontranscribed regions of the genome, is defined as faster repair of the transcribed strand versus the nontranscribed strand in transcribed genes. The phenomenon, universal in model organisms including Escherichia coli, yeast, Arabidopsis, mice, and humans, involves a translocase that interacts with both RNA polymerase stalled at damage in the transcribed strand and nucleotide excision repair proteins to accelerate repair. Drosophila, a notable exception, exhibits TCR but lacks an obvious TCR translocase. Mutations inactivating TCR genes cause increased damage-induced mutagenesis in E. coli and severe neurological and UV sensitivity syndromes in humans. To date, only E. coli TCR has been reconstituted in vitro with purified proteins. Detailed investigations of TCR using genome-wide next-generation sequencing methods, cryo-electron microscopy, single-molecule analysis, and other approaches have revealed fascinating mechanisms.

转录偶联修复(Transcription-coupled repair, TCR)是指哺乳动物基因组转录区与非转录区相比,紫外线诱导的环丁烷嘧啶二聚体的优先核苷酸切除修复,它被定义为转录基因中转录链比非转录链修复得更快。这种现象普遍存在于大肠杆菌、酵母、拟南芥、小鼠和人类等模式生物中,涉及一种转座酶,它与转录链损伤处停滞的RNA聚合酶和核苷酸切除修复蛋白相互作用,以加速修复。果蝇是一个明显的例外,它们表现出TCR,但缺乏明显的TCR转位酶。灭活TCR基因的突变导致大肠杆菌中损伤诱导的突变增加,并导致人类出现严重的神经系统和紫外线敏感性综合征。迄今为止,只有大肠杆菌TCR在体外用纯化蛋白重建。利用下一代全基因组测序方法、低温电子显微镜、单分子分析和其他方法对TCR进行的详细研究揭示了令人着迷的机制。
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引用次数: 6
3'-End Processing of Eukaryotic mRNA: Machinery, Regulation, and Impact on Gene Expression. 真核 mRNA 的 3'-End 处理:机械、调控和对基因表达的影响。
IF 12.1 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 Epub Date: 2023-03-31 DOI: 10.1146/annurev-biochem-052521-012445
Vytautė Boreikaitė, Lori A Passmore

Formation of the 3' end of a eukaryotic mRNA is a key step in the production of a mature transcript. This process is mediated by a number of protein factors that cleave the pre-mRNA, add a poly(A) tail, and regulate transcription by protein dephosphorylation. Cleavage and polyadenylation specificity factor (CPSF) in humans, or cleavage and polyadenylation factor (CPF) in yeast, coordinates these enzymatic activities with each other, with RNA recognition, and with transcription. The site of pre-mRNA cleavage can strongly influence the translation, stability, and localization of the mRNA. Hence, cleavage site selection is highly regulated. The length of the poly(A) tail is also controlled to ensure that every transcript has a similar tail when it is exported from the nucleus. In this review, we summarize new mechanistic insights into mRNA 3'-end processing obtained through structural studies and biochemical reconstitution and outline outstanding questions in the field.

真核生物 mRNA 3' 端的形成是产生成熟转录本的关键步骤。这一过程由多种蛋白因子介导,它们可裂解前 mRNA,添加多聚(A)尾,并通过蛋白去磷酸化调节转录。人类的裂解和多聚腺苷酸化特异性因子(CPSF)或酵母的裂解和多聚腺苷酸化因子(CPF)可协调这些酶活性、RNA 识别和转录。前 mRNA 的裂解位点会严重影响 mRNA 的翻译、稳定性和定位。因此,裂解位点的选择受到高度调控。聚(A)尾的长度也受到控制,以确保每个转录本从细胞核输出时都有相似的尾部。在这篇综述中,我们总结了通过结构研究和生化重组获得的关于 mRNA 3'-end 处理的新的机理认识,并概述了该领域的未决问题。
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引用次数: 0
Thiolase: A Versatile Biocatalyst Employing Coenzyme A-Thioester Chemistry for Making and Breaking C-C Bonds. 硫醇酶:一种多功能生物催化剂,利用辅酶A-硫酯化学来制造和破坏C-C键。
IF 16.6 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 DOI: 10.1146/annurev-biochem-052521-033746
Rajesh K Harijan, Subhadra Dalwani, Tiila-Riikka Kiema, Rajaram Venkatesan, Rik K Wierenga

Thiolases are CoA-dependent enzymes that catalyze the thiolytic cleavage of 3-ketoacyl-CoA, as well as its reverse reaction, which is the thioester-dependent Claisen condensation reaction. Thiolases are dimers or tetramers (dimers of dimers). All thiolases have two reactive cysteines: (a) a nucleophilic cysteine, which forms a covalent intermediate, and (b) an acid/base cysteine. The best characterized thiolase is the Zoogloea ramigera thiolase, which is a bacterial biosynthetic thiolase belonging to the CT-thiolase subfamily. The thiolase active site is also characterized by two oxyanion holes, two active site waters, and four catalytic loops with characteristic amino acid sequence fingerprints. Three thiolase subfamilies can be identified, each characterized by a unique sequence fingerprint for one of their catalytic loops, which causes unique active site properties. Recent insights concerning the thiolase reaction mechanism, as obtained from recent structural studies, as well as from classical and recent enzymological studies, are addressed, and open questions are discussed.

硫酶是辅酶a依赖的酶,催化3-酮酰基辅酶a的硫解裂解及其逆反应,即硫酯依赖的Claisen缩合反应。硫硫酶是二聚体或四聚体(二聚体的二聚体)。所有硫酶都有两种活性半胱氨酸:(a)形成共价中间体的亲核半胱氨酸和(b)酸/碱半胱氨酸。最具特征的硫酶是Zoogloea ramigera硫酶,它是一种细菌生物合成硫酶,属于ct硫酶亚家族。巯基酶活性位点还具有两个氧阴离子空穴、两个活性位点水和四个具有特征氨基酸序列指纹图谱的催化环。可以确定三个硫硫酶亚家族,每个亚家族都具有其催化环的独特序列指纹,这导致独特的活性位点性质。从最近的结构研究以及从经典和最近的酶学研究中获得的关于硫硫酶反应机制的最新见解得到了解决,并讨论了悬而未决的问题。
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引用次数: 1
Mechanism of Radical Initiation in the Radical SAM Enzyme Superfamily. 自由基SAM酶超家族中自由基起始机制研究。
IF 12.1 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 Epub Date: 2023-04-04 DOI: 10.1146/annurev-biochem-052621-090638
Brian M Hoffman, William E Broderick, Joan B Broderick

Radical S-adenosylmethionine (SAM) enzymes use a site-differentiated [4Fe-4S] cluster and SAM to initiate radical reactions through liberation of the 5'-deoxyadenosyl (5'-dAdo•) radical. They form the largest enzyme superfamily, with more than 700,000 unique sequences currently, and their numbers continue to grow as a result of ongoing bioinformatics efforts. The range of extremely diverse, highly regio- and stereo-specific reactions known to be catalyzed by radical SAM superfamily members is remarkable. The common mechanism of radical initiation in the radical SAM superfamily is the focus of this review. Most surprising is the presence of an organometallic intermediate, Ω, exhibiting an Fe-C5'-adenosyl bond. Regioselective reductive cleavage of the SAM S-C5' bond produces 5'-dAdo• to form Ω, with the regioselectivity originating in the Jahn-Teller effect. Ω liberates the free 5'-dAdo• as the catalytically active intermediate through homolysis of the Fe-C5' bond, in analogy to Co-C5' bond homolysis in B12, which was once viewed as biology's choice of radical generator.

自由基s -腺苷蛋氨酸(SAM)酶利用一个位点分化的[4Fe-4S]簇和SAM通过释放5'-脱氧腺苷(5'-dAdo•)自由基来引发自由基反应。它们形成了最大的酶超家族,目前有超过70万个独特的序列,并且由于正在进行的生物信息学努力,它们的数量还在继续增长。已知由自由基SAM超家族成员催化的极其多样化,高度区域特异性和立体特异性的反应范围是显着的。本文就自由基SAM超家族中自由基起始的共同机制作一综述。最令人惊讶的是有机金属中间体Ω的存在,显示出Fe-C5'-腺苷键。SAM S-C5'键的区域选择性还原裂解产生5'-dAdo•形成Ω,其区域选择性源于Jahn-Teller效应。Ω通过Fe-C5'键的均裂释放游离的5'-dAdo•作为催化活性中间体,类似于B12中的Co-C5'键的均裂,这一度被认为是生物学上自由基产生的选择。
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引用次数: 0
Mitochondrial DNA Release in Innate Immune Signaling. 先天性免疫信号中的线粒体 DNA 释放
IF 12.1 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 Epub Date: 2023-03-31 DOI: 10.1146/annurev-biochem-032620-104401
Laura E Newman, Gerald S Shadel

According to the endosymbiotic theory, most of the DNA of the original bacterial endosymbiont has been lost or transferred to the nucleus, leaving a much smaller (∼16 kb in mammals), circular molecule that is the present-day mitochondrial DNA (mtDNA). The ability of mtDNA to escape mitochondria and integrate into the nuclear genome was discovered in budding yeast, along with genes that regulate this process. Mitochondria have emerged as key regulators of innate immunity, and it is now recognized that mtDNA released into the cytoplasm, outside of the cell, or into circulation activates multiple innate immune signaling pathways. Here, we first review the mechanisms through which mtDNA is released into the cytoplasm, including several inducible mitochondrial pores and defective mitophagy or autophagy. Next, we cover how the different forms of released mtDNA activate specific innate immune nucleic acid sensors and inflammasomes. Finally, we discuss how intracellular and extracellular mtDNA release, including circulating cell-free mtDNA that promotes systemic inflammation, are implicated in human diseases, bacterial and viral infections, senescence and aging.

根据内共生理论,原始细菌内共生体的大部分 DNA 已丢失或转移到细胞核中,只剩下一个小得多(哺乳动物为 16 kb)的环状分子,这就是今天的线粒体 DNA(mtDNA)。在萌芽酵母中发现了 mtDNA 逃离线粒体并整合到核基因组中的能力,以及调控这一过程的基因。线粒体已成为先天性免疫的关键调节器,现在人们认识到,释放到细胞质、细胞外或血液循环中的 mtDNA 会激活多种先天性免疫信号通路。在这里,我们首先回顾了 mtDNA 释放到细胞质中的机制,包括几种可诱导的线粒体孔和有缺陷的有丝分裂或自噬。接下来,我们将介绍释放的不同形式的 mtDNA 如何激活特定的先天性免疫核酸传感器和炎性体。最后,我们将讨论细胞内和细胞外 mtDNA 的释放(包括促进全身炎症的循环细胞游离 mtDNA)如何与人类疾病、细菌和病毒感染、衰老和老化有关。
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引用次数: 0
Rubisco Function, Evolution, and Engineering. Rubisco功能,进化和工程。
IF 16.6 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-20 DOI: 10.1146/annurev-biochem-040320-101244
Noam Prywes, Naiya R Phillips, Owen T Tuck, Luis E Valentin-Alvarado, David F Savage

Carbon fixation is the process by which CO2 is converted from a gas into biomass. The Calvin-Benson-Bassham cycle (CBB) is the dominant carbon-consuming pathway on Earth, driving >99.5% of the ∼120 billion tons of carbon that are converted to sugar by plants, algae, and cyanobacteria. The carboxylase enzyme in the CBB, ribulose-1,5-bisphosphate carboxylase/oxygenase (rubisco), fixes one CO2 molecule per turn of the cycle into bioavailable sugars. Despite being critical to the assimilation of carbon, rubisco's kinetic rate is not very fast, limiting flux through the pathway. This bottleneck presents a paradox: Why has rubisco not evolved to be a better catalyst? Many hypothesize that the catalytic mechanism of rubisco is subject to one or more trade-offs and that rubisco variants have been optimized for their native physiological environment. Here, we review the evolution and biochemistry of rubisco through the lens of structure and mechanism in order to understand what trade-offs limit its improvement. We also review the many attempts to improve rubisco itself and thereby promote plant growth.

固碳是将二氧化碳从气体转化为生物质的过程。卡尔文-本森-巴萨姆循环(CBB)是地球上主要的碳消耗途径,在植物、藻类和蓝藻转化为糖的约1200亿吨碳中,有99.5%以上是由卡尔文-本森-巴萨姆循环驱动的。CBB中的羧化酶,核酮糖-1,5-二磷酸羧化酶/加氧酶(rubisco),在每一轮循环中将一个CO2分子固定为生物可利用的糖。尽管rubisco对碳的同化至关重要,但它的动力学速率不是很快,限制了通过该途径的通量。这个瓶颈提出了一个悖论:为什么rubisco没有进化成更好的催化剂?许多人假设rubisco的催化机制受到一个或多个权衡的影响,并且rubisco变体已经针对其原生生理环境进行了优化。在这里,我们从结构和机制的角度回顾rubisco的进化和生物化学,以了解哪些权衡限制了它的改进。我们也回顾了许多尝试改善rubisco本身,从而促进植物生长。
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引用次数: 7
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Annual review of biochemistry
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