Endoreplication: The Good, the Bad, and the Ugly Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-19 Zhiqiang Shu, Sarayu Row, Wu-Min Deng
To battle adverse internal and external conditions and maintain homeostasis, diploid organisms employ various cellular processes, such as proliferation and apoptosis. In some tissues, an alternative mechanism, endoreplication, is employed toward similar goals. Endoreplication is an evolutionarily conserved cell cycle program during which cells replicate their genomes without division, resulting in polyploid cells. Importantly, endoreplication is reported to be indispensable for normal development and organ formation across various organisms, from fungi to humans. In recent years, more attention has been drawn to delineating its connections to wound healing and tumorigenesis. In this Review, we discuss mechanisms of endoreplication and polyploidization, their essential and positive roles in normal development and tissue homeostasis, and the relationship between polyploidy and cancer.
BAX and BAK at the Gates of Innate Immunity Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-16 Lorenzo Galluzzi, Claire Vanpouille-Box
Large BAX/BAK pores that form during apoptosis enable mitochondrial nucleoids to access the cytosol, potentially leading to inflammatory signaling via CGAS. Under physiological conditions, however, BAX/BAK-dependent caspase activation rapidly dismantles dying cells to prevent inflammatory responses. BAX and BAK operate at the interface between apoptotic signaling and innate immunity control.
The Force Is Strong with This One: Metabolism (Over)powers Stem Cell Fate Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-16 Peng Wei, Katja K. Dove, Claire Bensard, John C. Schell, Jared Rutter
Compared to their differentiated progeny, stem cells are often characterized by distinct metabolic landscapes that emphasize anaerobic glycolysis and a lower fraction of mitochondrial carbohydrate oxidation. Until recently, the metabolic program of stem cells had been thought to be a byproduct of the environment, rather than an intrinsic feature determined by the cell itself. However, new studies highlight the impact of metabolic behavior on the maintenance and function of intestinal stem cells and hair follicle stem cells. This Review summarizes and discusses the evidence that metabolism is not a mere consequence of, but rather influential on stem cell fate.
Apoptotic Caspases: Multiple or Mistaken Identities? Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-15 Kate McArthur, Benjamin T. Kile
The mitochondrial caspase cascade was originally thought to be required for apoptotic death driven by Bak/Bax-mediated intrinsic apoptosis. It has also been ascribed several ‘non-apoptotic’ functions, including differentiation, proliferation, and cellular reprogramming. Recent work has demonstrated that, during apoptosis, the caspase cascade suppresses damage-associated molecular pattern (DAMP)-initiated production of cytokines such as type I interferon by the dying cell. The caspase cascade is not required for death to occur; instead, it shapes the immunogenic properties of the apoptotic cell. This raises questions about the role of apoptotic caspases in regulating DAMP signaling more generally, puts a new perspective on their non-apoptotic functions, and suggests that pharmacological caspase inhibitors might find new applications as antiviral or anticancer agents.
Eukaryotic RNA 5′-End NAD+ Capping and DeNADding Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-12 Megerditch Kiledjian
A hallmark of eukaryotic mRNAs has long been the 5′-end m7G cap. This paradigm was recently amended by recent reports that Saccharomyces cerevisiae and mammalian cells also contain mRNAs carrying a novel nicotinamide adenine dinucleotide (NAD+) cap at their 5′-end. The presence of an NAD+ cap on mRNA uncovers a previously unknown mechanism for controlling gene expression through nucleotide metabolite-directed mRNA turnover. In contrast to the m7G cap that stabilizes mRNA, the NAD+ cap targets RNA for rapid decay in mammalian cells through the DXO non-canonical decapping enzyme which removes intact NAD+ from RNA in a process termed ‘deNADding’. This review highlights the identification of NAD+ caps, their mode of addition, and their functional significance in cells.
Translational Control by Prion-like Proteins Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-09 Liying Li, J.P. McGinnis, Kausik Si
Prion-like proteins overlap with intrinsically disordered and low-complexity sequence families. These proteins are widespread, especially among mRNA-binding proteins. A salient feature of these proteins is the ability to form protein assemblies with distinct biophysical and functional properties. While prion-like proteins are involved in myriad of cellular processes, we propose potential roles for protein assemblies in regulated protein synthesis. Since proteins are the ultimate functional output of gene expression, when, where, and how much of a particular protein is made dictates the functional state of a cell. Recent finding suggests that the prion-like proteins offer unique advantages in translation regulation and also raises questions regarding formation and regulation of protein assemblies.
Clustering on Membranes: Fluctuations and More Trends Cell Biol. (IF 15.333) Pub Date : 2018-03-01 Ludger Johannes, Weria Pezeshkian, John H. Ipsen, Julian C. Shillcock
Clustering of extracellular ligands and proteins on the plasma membrane is required to perform specific cellular functions, such as signaling and endocytosis. Attractive forces that originate in perturbations of the membrane’s physical properties contribute to this clustering, in addition to direct protein–protein interactions. However, these membrane-mediated forces have not all been equally considered, despite their importance. In this review, we describe how line tension, lipid depletion, and membrane curvature contribute to membrane-mediated clustering. Additional attractive forces that arise from protein-induced perturbation of a membrane’s fluctuations are also described. This review aims to provide a survey of the current understanding of membrane-mediated clustering and how this supports precise biological functions.
Control of Mechanotransduction by Molecular Clutch Dynamics Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-26 Alberto Elosegui-Artola, Xavier Trepat, Pere Roca-Cusachs
The linkage of cells to their microenvironment is mediated by a series of bonds that dynamically engage and disengage, in what has been conceptualized as the molecular clutch model. Whereas this model has long been employed to describe actin cytoskeleton and cell migration dynamics, it has recently been proposed to also explain mechanotransduction (i.e., the process by which cells convert mechanical signals from their environment into biochemical signals). Here we review the current understanding on how cell dynamics and mechanotransduction are driven by molecular clutch dynamics and its master regulator, the force loading rate. Throughout this Review, we place a specific emphasis on the quantitative prediction of cell response enabled by combined experimental and theoretical approaches.
Hallmarks of Cellular Senescence Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-21 Alejandra Hernandez-Segura, Jamil Nehme, Marco Demaria
Cellular senescence is a permanent state of cell cycle arrest that promotes tissue remodeling during development and after injury, but can also contribute to the decline of the regenerative potential and function of tissues, to inflammation, and to tumorigenesis in aged organisms. Therefore, the identification, characterization, and pharmacological elimination of senescent cells have gained attention in the field of aging research. However, the nonspecificity of current senescence markers and the existence of different senescence programs strongly limit these tasks. Here, we describe the molecular regulators of senescence phenotypes and how they are used for identifying senescent cells in vitro and in vivo. We also highlight the importance that these levels of regulations have in the development of therapeutic targets.
Recent Advances in Lgr5+ Stem Cell Research Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-21 Carly Leung, Si Hui Tan, Nick Barker
The discovery of leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5) as both a marker of adult stem cells and a critical modulator of their activity via its role as an effector of Wnt/R-spondin (Rspo) signaling has driven major advances in our understanding of stem cell biology during homeostasis, regeneration, and disease. Exciting new mouse and organoid culture models developed to study the endogenous behavior of Lgr5-expressing cells in health and disease settings have revealed the existence of facultative stem cell populations responsible for tissue regeneration, cancer stem cells (CSCs) driving metastasis in the gut, and Lgr5+ niche cells in the lung. Here we review these recent advances and discuss their impact on efforts to harness the therapeutic potential of adult stem cells and their cancer counterparts in the clinic.
GCN5L1/BLOS1 Links Acetylation, Organelle Remodeling, and Metabolism Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-21 Iain Scott, Lingdi Wang, Kaiyuan Wu, Dharendra Thapa, Michael N. Sack
General control of amino acid synthesis 5 (GCN5) like-1 (GCN5L1) was identified as a novel gene with sequence homology to the histone acetyltransferase Gcn5. Subsequent protein-interaction studies identified GCN5L1 as a subunit of the multiprotein lysosome biogenesis complex, resulting in an alternative designation as biogenesis of lysosome-related organelle complex 1 subunit 1 (BLOS1 or BLOC1S1). Despite the distinct nomenclatures, GCN5L1/BLOS1 has been shown to play crucial roles in mitochondria, endosomes, lysosomes, and synaptic vesicle precursors (SVPs). GCN5L1/BLOS1 controls mitochondrial protein acetylation, modulates metabolic pathways, and orchestrates retrograde mitochondria-to-nucleus signaling. It also contributes to endosome–lysosome and vesicle trafficking and to endolysosomal function. Here we discuss the intracellular roles of GCN5L1/BLOS1 in the hope of linking mitochondria-centric effects to cytosolic vesicle biology.
Molecular Cogs: Interplay between Circadian Clock and Cell Cycle Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-19 Jonathan Gaucher, Emilie Montellier, Paolo Sassone-Corsi
The cell cycle and the circadian clock operate as biological oscillators whose timed functions are tightly regulated. Accumulating evidence illustrates the presence of molecular links between these two oscillators. This mutual interplay utilizes various coupling mechanisms, such as the use of common regulators. The connection between these two cyclic systems has unique interest in the context of aberrant cell proliferation since both of these oscillators are frequently misregulated in cancer cells. Further studies will provide deeper understanding of the detailed molecular connections between the cell cycle and the circadian clock and may also serve as a basis for the design of innovative therapeutic strategies.
Rethinking Phagocytes: Clues from the Retina and Testes Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-14 Kristen K. Penberthy, Jeffrey J. Lysiak, Kodi S. Ravichandran
Specialized phagocytes are a newly appreciated classification of phagocyte that currently encompasses Sertoli cells (SCs) of the testes and the retinal pigment epithelial cells (RPE) of the retina. While these cells support very different tissues, they have a striking degree of similarity both as phagocytes and in ways that go beyond cell clearance. The clearance of apoptotic germ cells, cell debris, and used photoreceptor outer segments are critical functions of these cells, and the unique nature of their clearance events make specialized phagocytes uniquely suited for studying the larger implications of cell clearance in vivo. The shared functions of specialized phagocytes could provide novel insights into how phagocytosis impacts tissue homeostasis and immune modulation. In this review, we examine the remarkable similarities between SCs and RPE as specialized phagocytes and the physiological effects of cell clearance within a tissue.
The Elusive P2X7 Macropore Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-10 Francesco Di Virgilio, Günther Schmalzing, Fritz Markwardt
ATP, which is released under pathological conditions and is considered a damage-associated molecular pattern (DAMP), activates P2X7 receptors (P2X7Rs), trimeric plasma membrane ion channels selective for small cations. P2X7Rs are partners in NOD-like receptor containing a pyrin (NLRP3) inflammasome activation and promoters of tumor cell growth. P2X7R overstimulation triggers the ATP-dependent opening of a nonselective plasma membrane pore, known as a ‘macropore’, which allows fluxes of large hydrophilic molecules. The pathophysiological functions of P2X7R are thought to be dependent on activation of this conductance pathway, yet its molecular identity is unknown. Recent reports show that P2X7R permeability to organic solutes is an early and intrinsic property of the channel itself. A better understanding of P2X7R-dependent changes in plasma membrane permeability will allow a rationale development of novel anti-inflammatory and anticancer drugs.
Calcium Dynamics as a Machine for Decoding Signals Trends Cell Biol. (IF 15.333) Pub Date : 2018-02-03 Carlotta Giorgi, Alberto Danese, Sonia Missiroli, Simone Patergnani, Paolo Pinton
Calcium (Ca2+) is considered one of the most-important biological cations, because it is implicated in cell physiopathology and cell fate through a finely tuned signaling system. In support of this notion, Ca2+ is the primary driver of cell proliferation and cell growth; however, it is also intimately linked to cell death. Functional abnormalities or mutations in proteins that mediate Ca2+ homeostasis usually lead to a plethora of diseases and pathogenic states, including cancer, heart failure, diabetes, and neurodegenerative disease. In this review, we examine recent discoveries in the highly localized nature of Ca2+-dependent signal transduction and its roles in cell fate, inflammasome activation, and synaptic transmission.
Cortactin: Cell Functions of A Multifaceted Actin-Binding Protein Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-20 Michael Schnoor, Theresia E. Stradal, Klemens Rottner
Cortactin fulfills many functions in various cell types. These functions have been considered to derive from its ability to activate the Actin-related protein 2/3 (Arp2/3) complex, and are regulated by post-translational modifications, including phosphorylation and acetylation. New evidence suggests that cortactin regulates cell migration by controlling the deposition of extracellular matrix proteins rather than lamellipodial Arp2/3 activation, and that cortactin also functions in GTPase signaling, vesicular trafficking, and actomyosin contractility. These recent new findings and concepts are relevant for physiological and pathological cell functions, but have not yet been put into mechanistic context. Here, we reconsider current thinking on cortactin functions in different cell types during health and disease, and discuss potential directions of future research in cortactin biology.
‘Disc-o-Fever’: Getting Down with Giardia’s Groovy Microtubule Organelle Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-15 Christopher Nosala, Kari D. Hagen, Scott C. Dawson
Protists have evolved a myriad of highly specialized cytoskeletal organelles that expand known functional capacities of microtubule (MT) polymers. One such innovation – the ventral disc – is a cup-shaped MT organelle that the parasite Giardia uses to attach to the small intestine of its host. The molecular mechanisms underlying the generation of suction-based forces by overall conformational changes of the disc remain unclear. The elaborate disc architecture is defined by novel proteins and complexes that decorate almost all disc MT protofilaments, and vary in composition and conformation along the length of the MTs. Future genetic, biochemical, and functional analyses of disc-associated proteins will be central toward understanding not only disc architecture and assembly, but also the overall disc conformational dynamics that promote attachment.
Reading m6A in the Transcriptome: m6A-Binding Proteins Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-02 Deepak P. Patil, Brian F. Pickering, Samie R. Jaffrey
N6-Methyladenosine (m6A) is the most prevalent post-transcriptional modification of eukaryotic mRNA and long noncoding RNA. m6A mediates its effects primarily by recruiting proteins, including the multiprotein eukaryotic initiation factor 3 complex and a set of proteins that contain the YTH domain. Here we describe the mechanisms by which YTH domain-containing proteins bind m6A and influence the fate of m6A-containing RNA in mammalian cells. We discuss the diverse, and occasionally contradictory, functions ascribed to these proteins and the emerging concepts that are influencing our understanding of these proteins and their effects on the epitranscriptome.
Cell-Autonomous Metabolic Reprogramming in Hypoxia Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-27 Luana Schito, Sergio Rey
Molecular oxygen (O2) is a universal electron acceptor that enables ATP synthesis through mitochondrial respiration in all metazoans. Consequently, hypoxia (low O2) has arisen as an organizing principle for cellular evolution, metabolism, and (patho)biology, eliciting a remarkable panoply of metabolic adaptations that trigger transcriptional, translational, post-translational, and epigenetic responses to determine cellular fitness. In this review we summarize current and emerging cell-autonomous molecular mechanisms that induce hypoxic metabolic reprogramming in health and disease.
Zebrafish Infection: From Pathogenesis to Cell Biology Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-21 Vincenzo Torraca, Serge Mostowy
The study of host–pathogen interactions has illuminated fundamental research avenues in both infection and cell biology. Zebrafish (Danio rerio) larvae are genetically tractable, optically accessible, and present a fully functional innate immune system with macrophages and neutrophils that mimic their mammalian counterparts. A wide variety of pathogenic bacteria have been investigated using zebrafish models, providing unprecedented resolution of the cellular response to infection in vivo. In this review, we illustrate how zebrafish models have contributed to our understanding of cellular microbiology by providing an in vivo platform to study host–pathogen interactions from the single cell to whole animal level. We also highlight discoveries made from zebrafish infection that hold great promise for translation into novel therapies for humans.
Wnt and Hedgehog: Secretion of Lipid-Modified Morphogens Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-10 Anup Parchure, Neha Vyas, Satyajit Mayor
Morphogens are signaling molecules produced by a localized source, specifying cell fate in a graded manner. The source secretes morphogens into the extracellular milieu to activate various target genes in an autocrine or paracrine manner. Here we describe various secreted forms of two canonical morphogens, the lipid-anchored Hedgehog (Hh) and Wnts, indicating the involvement of multiple carriers in the transport of these morphogens. These different extracellular secreted forms are likely to have distinct functions. Here we evaluate newly identified mechanisms that morphogens use to traverse the required distance to activate discrete paracrine signaling.
Heterotypic Ubiquitin Chains: Seeing is Believing Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-27 Alexandra Stolz, Ivan Dikic
The biological diversity of ubiquitination resides in the multivalent nature of linkage-specific homotypic and heterotypic ubiquitin (Ub) chains. A recent publication by Yau et al. in Cell describes the development of K11/K48-bispecific antibodies and a physiological role for K11/K48 heterotypic chains in regulation of the cell cycle and clearance of aggregated proteins.
The Importance of Kinase–Phosphatase Integration: Lessons from Mitosis Trends Cell Biol. (IF 15.333) Pub Date : 2017-10-28 Lendert Gelens, Junbin Qian, Mathieu Bollen, Adrian T. Saurin
Kinases and phosphatases work antagonistically to control the behaviour of individual substrate molecules. This can be incorrectly extrapolated to imply that they also work antagonistically on the signals or processes that these molecules control. In fact, in many situations kinases and phosphatases work together to positively drive signal responses. We explain how this ‘cooperativity’ is critical for setting the amplitude, localisation, timing, and shape of phosphorylation signals. We use mitosis to illustrate why these properties are important for controlling mitotic entry, sister chromatid cohesion, kinetochore–microtubule attachments, the spindle assembly checkpoint, mitotic spindle elongation, and mitotic exit. These examples provide a rationale to explain how complex signalling behaviour could rely on similar types of integration within many other biological processes.
Kinetochore Function from the Bottom Up Trends Cell Biol. (IF 15.333) Pub Date : 2017-10-03 Stephen M. Hinshaw, Stephen C. Harrison
During a single human lifetime, nearly one quintillion chromosomes separate from their sisters and transit to their destinations in daughter cells. Unlike DNA replication, chromosome segregation has no template, and, unlike transcription, errors frequently lead to a total loss of cell viability. Rapid progress in recent years has shown how kinetochores enable faithful execution of this process by connecting chromosomal DNA to microtubules. These findings have transformed our idea of kinetochores from cytological features to immense molecular machines and now allow molecular interpretation of many long-appreciated kinetochore functions. In this review we trace kinetochore protein connectivity from chromosomal DNA to microtubules, relating new findings to important points of regulation and function.
Nuclear Lamins: Thin Filaments with Major Functions Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-08 Rebecca de Leeuw, Yosef Gruenbaum, Ohad Medalia
The nuclear lamina is a nuclear peripheral meshwork that is mainly composed of nuclear lamins, although a small fraction of lamins also localizes throughout the nucleoplasm. Lamins are classified as type V intermediate filament (IF) proteins. Mutations in lamin genes cause at least 15 distinct human diseases, collectively termed laminopathies, including muscle, metabolic, and neuronal diseases, and can cause accelerated aging. Most of these mutations are in the LMNA gene encoding A-type lamins. A growing number of nuclear proteins are known to bind lamins and are implicated in both nuclear and cytoskeletal organization, mechanical stability, chromatin organization, signaling, gene regulation, genome stability, and cell differentiation. Recent studies reveal the organization of the lamin filament meshwork in somatic cells where they assemble as tetramers in cross-section of the filaments.
Humanity in a Dish: Population Genetics with iPSCs Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-23 Curtis R. Warren, Chad A. Cowan
Induced pluripotent stem cells (iPSCs) are powerful tools for investigating the relationship between genotype and phenotype. Recent publications have described iPSC cohort studies of common genetic variants and their effects on gene expression and cellular phenotypes. These in vitro quantitative trait locus (QTL) studies are the first experiments in a new paradigm with great potential: iPSC-based functional population genetic studies. iPSC collections from large cohorts are currently under development to facilitate the next wave of these studies, which have the potential to discover the effects of common genetic variants on cellular phenotypes and to uncover the molecular basis of common genetic diseases. Here, we describe the recent advances in this developing field, and provide a road map for future in vitro functional population genetic studies and trial-in-a-dish experiments.
Proinflammatory Signals as Fuel for the Fire of Hematopoietic Stem Cell Emergence Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-04 Raquel Espin-Palazon, Bart Weijts, Victor Mulero, David Traver
Hematopoietic stem cells (HSCs) have the extraordinary ability to both self-renew and generate all mature blood cell lineages. The ability to produce or expand patient-derived HSCs in vitro would greatly improve the outcome for patients with blood disorders that are currently treated with allogeneic HSC transplantation. Many laboratories have been working to identify the signals required for HSC emergence in their native environments to apply this knowledge in vitro. Recently, several signals traditionally known to underlie classical inflammation have emerged as essential regulators of HSC development. In this review we synthesize the findings that have established inflammatory cues as key regulators of HSC development.
Phosphatidic Acid and Cardiolipin Coordinate Mitochondrial Dynamics Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-11 Shoichiro Kameoka, Yoshihiro Adachi, Koji Okamoto, Miho Iijima, Hiromi Sesaki
Membrane organelles comprise both proteins and lipids. Remodeling of these membrane structures is controlled by interactions between specific proteins and lipids. Mitochondrial structure and function depend on regulated fusion and the division of both the outer and inner membranes. Here we discuss recent advances in the regulation of mitochondrial dynamics by two critical phospholipids, phosphatidic acid (PA) and cardiolipin (CL). These two lipids interact with the core components of mitochondrial fusion and division (Opa1, mitofusin, and Drp1) to activate and inhibit these dynamin-related GTPases. Moreover, lipid-modifying enzymes such as phospholipases and lipid phosphatases may organize local lipid composition to spatially and temporarily coordinate a balance between fusion and division to establish mitochondrial morphology.
Bacterial Subversion of COG-Dependent Membrane Traffic Trends Cell Biol. (IF 15.333) Pub Date : 2017-10-04 Lee Dolat, Raphael H. Valdivia
Intracellular bacterial pathogens thrive within eukaryotic cells by interacting with a range of organelles to establish a replicative niche. In a new study in Cell Host and Microbe, Miller et al. identify a Brucella abortus effector that subverts membrane and protein transport to the Golgi apparatus to promote bacterial replication.
Vav1: Friend and Foe of Cancer Trends Cell Biol. (IF 15.333) Pub Date : 2017-10-30 Fukun Guo, Yi Zheng
A recent study shows that the protumorigenic guanine nucleotide exchange factor (GEF) Vav1 functions as a tumor suppressor in T cell acute lymphoblastic leukemia (T-ALL) through its ability to complex with the Cbl-b ubiquitin ligase and the intracellular domain of Notch1 (ICN1) and to promote ICN1 degradation. Vav1can act as a double-edged sword in tumorigenesis.
Immunosurveillance of Malignant Cells with Complex Karyotypes Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-19 Alejandro López-Soto, Segundo Gonzalez, Carlos López-Larrea, Guido Kroemer
A wide array of cell-intrinsic surveillance mechanisms maintains the homeostasis of dividing cells and the integrity of the genome. Accumulating evidence also supports a role for cell-extrinsic mechanisms. Among them, the immune system, together with cell-autonomous checkpoint processes, eliminates cells that harbor unbalanced karyotypes generated by mitotic defects.
Plant Cytokinesis: Terminology for Structures and Processes Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-21 Andrei Smertenko, Farhah Assaad, František Baluška, Magdalena Bezanilla, Henrik Buschmann, Georgia Drakakaki, Marie-Theres Hauser, Marcel Janson, Yoshinobu Mineyuki, Ian Moore, Sabine Müller, Takashi Murata, Marisa S. Otegui, Emmanuel Panteris, Carolyn Rasmussen, Anne-Catherine Schmit, Jozef Šamaj, Lacey Samuels, Viktor Žárský
Plant cytokinesis is orchestrated by a specialized structure, the phragmoplast. The phragmoplast first occurred in representatives of Charophyte algae and then became the main division apparatus in land plants. Major cellular activities, including cytoskeletal dynamics, vesicle trafficking, membrane assembly, and cell wall biosynthesis, cooperate in the phragmoplast under the guidance of a complex signaling network. Furthermore, the phragmoplast combines plant-specific features with the conserved cytokinetic processes of animals, fungi, and protists. As such, the phragmoplast represents a useful system for understanding both plant cell dynamics and the evolution of cytokinesis. We recognize that future research and knowledge transfer into other fields would benefit from standardized terminology. Here, we propose such a lexicon of terminology for specific structures and processes associated with plant cytokinesis.
Rethinking HSF1 in Stress, Development, and Organismal Health Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-07 Jian Li, Johnathan Labbadia, Richard I. Morimoto
The heat shock response (HSR) was originally discovered as a transcriptional response to elevated temperature shock and led to the identification of heat shock proteins and heat shock factor 1 (HSF1). Since then HSF1 has been shown to be important for combating other forms of environmental perturbations as well as genetic variations that cause proteotoxic stress. The HSR has long been thought to be an absolute response to conditions of cell stress and the primary mechanism by which HSF1 promotes organismal health by preventing protein aggregation and subsequent proteome imbalance. Accumulating evidence now shows that HSF1, the central player in the HSR, is regulated according to specific cellular requirements through cell-autonomous and non-autonomous signals, and directs transcriptional programs distinct from the HSR during development and in carcinogenesis. We discuss here these ‘non-canonical’ roles of HSF1, its regulation in diverse conditions of development, reproduction, metabolism, and aging, and posit that HSF1 serves to integrate diverse biological and pathological responses.
Ki-67 and the Chromosome Periphery Compartment in Mitosis Trends Cell Biol. (IF 15.333) Pub Date : 2017-08-23 Daniel G. Booth, William C. Earnshaw
The chromosome periphery is a complex network of proteins and RNA molecules (many derived from nucleoli) that covers the outer surface of chromosomes and whose function remains mysterious. Although it was first described over 130 years ago, technological advances and the recent discovery that Ki-67 acts as an organiser of this region have allowed the chromosome periphery to be dissected in previously unattainable detail, leading to a revival of interest in this obscure chromosomal compartment. Here, we review the most recent advances into the composition, structure and function of the chromosome periphery, discuss possible roles of Ki-67 during mitosis and consider why this structure is likely to remain the focus of ongoing attention in the future.
Rebuilding Chromosomes After Catastrophe: Emerging Mechanisms of Chromothripsis Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-09 Peter Ly, Don W. Cleveland
Cancer genome sequencing has identified chromothripsis, a complex class of structural genomic rearrangements involving the apparent shattering of an individual chromosome into tens to hundreds of fragments. An initial error during mitosis, producing either chromosome mis-segregation into a micronucleus or chromatin bridge interconnecting two daughter cells, can trigger the catastrophic pulverization of the spatially isolated chromosome. The resultant chromosomal fragments are religated in random order by DNA double-strand break repair during the subsequent interphase. Chromothripsis scars the cancer genome with localized DNA rearrangements that frequently generate extensive copy number alterations, oncogenic gene fusion products, and/or tumor suppressor gene inactivation. Here we review emerging mechanisms underlying chromothripsis with a focus on the contribution of cell division errors caused by centromere dysfunction.
Neural Glycosylphosphatidylinositol-Anchored Proteins in Synaptic Specification Trends Cell Biol. (IF 15.333) Pub Date : 2017-07-22 Ji Won Um, Jaewon Ko
Glycosylphosphatidylinositol (GPI)-anchored proteins are a specialized class of lipid-associated neuronal membrane proteins that perform diverse functions in the dynamic control of axon guidance, synaptic adhesion, cytoskeletal remodeling, and localized signal transduction, particularly at lipid raft domains. Recent studies have demonstrated that a subset of GPI-anchored proteins act as critical regulators of synapse development by modulating specific synaptic adhesion pathways via direct interactions with key synapse-organizing proteins. Additional studies have revealed that alteration of these regulatory mechanisms may underlie various brain disorders. In this review, we highlight the emerging role of GPI-anchored proteins as key synapse organizers that aid in shaping the properties of various types of synapses and circuits in mammals.
Lymphocyte Fate and Metabolism: A Clonal Balancing Act Trends Cell Biol. (IF 15.333) Pub Date : 2017-08-14 Simone A. Nish, Wen-Hsuan W. Lin, Steven L. Reiner
Activated lymphocytes perform a clonal balancing act, yielding a daughter cell that differentiates owing to intense PI3K signaling, alongside a self-renewing sibling cell with blunted anabolic signaling. Divergent cellular anabolism versus catabolism is emerging as a feature of several developmental and regenerative paradigms. Metabolism can dictate cell fate, in part, because lineage-specific regulators are embedded in the circuitry of conserved metabolic switches. Unequal transmission of PI3K signaling during regenerative divisions is reminiscent of compartmentalized PI3K activity during directed motility or polarized information flow in non-dividing cells. The diverse roles of PI3K pathways in membrane traffic, cell polarity, metabolism, and gene expression may have converged to instruct sibling cell feast and famine, thereby enabling clonal differentiation alongside self-renewal.
Sensing of Cytoskeletal Forces by Asymmetric Adherens Junctions Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-28 Tsveta S. Malinova, Stephan Huveneers
Within tissues, key cellular adaptations occur via mechanotransduction responses at cell–cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell–cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell–cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease.
Microtubule-Organizing Centers: Towards a Minimal Parts List Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-21 Joel Paz, Jens Lüders
Despite decades of molecular analysis of the centrosome, an important microtubule-organizing center (MTOC) of animal cells, the molecular basis of microtubule organization remains obscure. A major challenge is the sheer complexity of the interplay of the hundreds of proteins that constitute the centrosome. However, this complexity owes not only to the centrosome’s role as a MTOC but also to the requirements of its duplication cycle and to various other functions such as the formation of cilia, the integration of various signaling pathways, and the organization of actin filaments. Thus, rather than using the parts lists to reconstruct the centrosome, we propose to identify the subset of proteins minimally needed to assemble a MTOC and to study this process at non-centrosomal sites.
Endothelial Cell Metabolism in Health and Disease Trends Cell Biol. (IF 15.333) Pub Date : 2017-11-16 Katerina Rohlenova, Koen Veys, Ines Miranda-Santos, Katrien De Bock, Peter Carmeliet
The metabolism of endothelial cells (ECs) has only recently been recognized as a driving force of angiogenesis. Metabolic pathways, such as glycolysis, fatty acid oxidation, and glutamine metabolism, have distinct, essential roles during vessel formation. Moreover, EC metabolism is markedly perturbed in pathologies such as cancer and diabetes. For instance, because tumor ECs increase glycolysis, lowering hyperglycolysis in tumor ECs induces therapeutic benefits in preclinical tumor models. Expanding our knowledge of how ECs alter their metabolism in disease could pave the way for novel therapeutic opportunities. In this review, we discuss the most recent insights into EC metabolism in health and disease, with emphasis on the changes in metabolism in the tumor endothelium.
Collapsing the Metabolic PON2zi Scheme in Pancreatic Ductal Adenocarcinoma Trends Cell Biol. (IF 15.333) Pub Date : 2017-10-04 Matyas Abel Tsegaye, Zachary T. Schafer
A hallmark of pancreatic ductal adenocarcinoma cancer (PDAC) cells is metabolic reprogramming that facilitates tumor progression. In a recent paper published in Molecular Cell, Nagarajan et al. discover that paraoxonase (PON)2 stimulates glucose transporter (GLUT)1-mediated glucose uptake, prevents AMP-activated protein kinase (AMPK)-mediated anoikis, and consequently promotes PDAC development and metastasis.
Mitochondrial Nanotunnels Trends Cell Biol. (IF 15.333) Pub Date : 2017-09-19 Amy E. Vincent, Doug M. Turnbull, Veronica Eisner, György Hajnóczky, Martin Picard
Insight into the regulation of complex physiological systems emerges from understanding how biological units communicate with each other. Recent findings show that mitochondria communicate at a distance with each other via nanotunnels, thin double-membrane protrusions that connect the matrices of non-adjacent mitochondria. Emerging evidence suggest that mitochondrial nanotunnels are generated by immobilized mitochondria and transport proteins. This review integrates data from the evolutionarily conserved structure and function of intercellular projections in bacteria with recent developments in mitochondrial imaging that permit nanotunnel visualization in eukaryotes. Cell type-specificity, timescales, and the selective size-based diffusion of biomolecules along nanotunnels are also discussed. The joining of individual mitochondria into dynamic networks of communicating organelles via nanotunnels and other mechanisms has major implications for organelle and cellular behaviors.
Apoptosis and Necroptosis as Host Defense Strategies to Prevent Viral Infection Trends Cell Biol. (IF 15.333) Pub Date : 2017-06-19 Megan H. Orzalli, Jonathan C. Kagan
Antiviral transcriptional responses and regulated cell death are crucial components of the host response to virus infection. However, in contrast to the signaling pathways that promote antiviral transcription, those that initiate cell death following virus infection are less understood. Several recent studies have identified pattern recognition receptors (PRRs) of the mammalian innate immune system that activate cell death pathways. These same receptors also have established roles in the induction of antiviral gene expression. In this review we discuss the mechanisms by which PRRs can serve dual roles as initiators of inflammatory gene expression and as inducers of apoptosis and necroptosis following virus infection.
Chromosome Intermingling: Mechanical Hotspots for Genome Regulation Trends Cell Biol. (IF 15.333) Pub Date : 2017-07-17 Caroline Uhler, G.V. Shivashankar
Cells sense physical and chemical signals from their local microenvironment and transduce them to the nucleus to regulate genomic programs. In this review, we first discuss different modes of mechanotransduction to the nucleus. We then highlight the role of the spatial organization of chromosomes for integrating these signals. In particular, we emphasize the importance of chromosome intermingling for gene regulation. We also discuss various geometric models and recent advances in microscopy and genomics that have allowed access to these nanoscale chromosome intermingling regions. Taken together, the recent work summarized in this review culminates in the hypothesis that chromosome intermingling regions are mechanical hotspots for genome regulation. Maintenance of such mechanical hotspots is crucial for cellular homeostasis, and alterations in them could be precursors for various cellular reprogramming events, including diseases.
Spatial and Temporal Control of Senescence Trends Cell Biol. (IF 15.333) Pub Date : 2017-08-17 Yoko Ito, Matthew Hoare, Masashi Narita
Cellular senescence is an autonomous tumor suppressor mechanism leading to stable cell cycle arrest. Senescent cells are highly secretory, driving a range of different functions through the senescence-associated secretory phenotype (SASP). Recent findings have suggested that the composition of the SASP is dynamically and spatially regulated and that the changing composition of the SASP can determine the beneficial and detrimental aspects of the senescence program, tipping the balance to either an immunosuppressive/profibrotic environment or proinflammatory/fibrolytic state. Here, we discuss the current understanding of the temporal and spatial regulation of the SASP and the novel finding of NOTCH signaling as a regulator of SASP composition.
Emerging Roles for the Lysosome in Lipid Metabolism Trends Cell Biol. (IF 15.333) Pub Date : 2017-08-30 Ashley M. Thelen, Roberto Zoncu
Precise regulation of lipid biosynthesis, transport, and storage is key to the homeostasis of cells and organisms. Cells rely on a sophisticated but poorly understood network of vesicular and nonvesicular transport mechanisms to ensure efficient delivery of lipids to target organelles. The lysosome stands at the crossroads of this network due to its ability to process and sort exogenous and endogenous lipids. The lipid-sorting function of the lysosome is intimately connected to its recently discovered role as a metabolic command-and-control center, which relays multiple nutrient cues to the master growth regulator, mechanistic target of rapamycin complex (mTORC)1 kinase. In turn, mTORC1 potently drives anabolic processes, including de novo lipid synthesis, while inhibiting lipid catabolism. Here, we describe the dual role of the lysosome in lipid transport and biogenesis, and we discuss how integration of these two processes may play important roles both in normal physiology and in disease.
Novel Structural Insights into GPCR–β-Arrestin Interaction and Signaling Trends Cell Biol. (IF 15.333) Pub Date : 2017-06-23 Ravi Ranjan, Hemlata Dwivedi, Mithu Baidya, Mohit Kumar, Arun K. Shukla
G protein-coupled receptors (GPCRs) are major signal recognition and transmission units in the plasma membrane. The interaction of activated and phosphorylated GPCRs with the multifunctional adaptor proteins β-arrestins (βarrs) is crucial for regulation of their signaling and functional outcomes. Over the past few years, a range of structural, biochemical, and cellular studies have revealed novel insights into GPCR–βarr interaction and signaling. Some of these findings have come as a surprise and therefore have the potential to significantly refine the conceptual framework of the GPCR–βarr system. Here we discuss these recent advances with particular emphasis on biphasic GPCR–βarr interaction, the formation of GPCR–G-protein–βarr supercomplexes, and receptor-specific conformational signatures in βarrs. We also underline the emerging research areas that are likely to be at the center stage of investigations in the coming years.
Metabolic Interactions in the Tumor Microenvironment Trends Cell Biol. (IF 15.333) Pub Date : 2017-07-19 Costas A. Lyssiotis, Alec C. Kimmelman
Tumors are dynamic pseudoorgans that contain numerous cell types interacting to create a unique physiology. Within this network, the malignant cells encounter many challenges and rewire their metabolic properties accordingly. Such changes can be experienced and executed autonomously or through interaction with other cells in the tumor. The focus of this review is on the remodeling of the tumor microenvironment that leads to pathophysiologic interactions that are influenced and shaped by metabolism. They include symbiotic nutrient sharing, nutrient competition, and the role of metabolites as signaling molecules. Examples of such processes abound in normal organismal physiology, and such heterocellular metabolic interactions are repurposed to support tumor metabolism and growth. The importance and ubiquity of these processes are just beginning to be realized, and insights into their role in tumor development and progression are being used to design new drug targets and cancer therapies.
Autophagy in Neurodegeneration: Can’t Digest It, Spit It Out! Trends Cell Biol. (IF 15.333) Pub Date : 2018-01-31 Valentin J.A. Barthet, Kevin M. Ryan
The autophagy-lysosome pathway maintains cellular homeostasis and protects against neurodegenerative disorders. Recent findings show that autophagy can be impaired in these diseases, and that the cell activates an alternative Golgi-mediated degradation pathway, leading to expulsion of toxic protein aggregates. Ultimately this process leads to nuclear breakdown and neuronal cell death.
Novel Insights into NDP52 Autophagy Receptor Functioning Trends Cell Biol. (IF 15.333) Pub Date : 2018-01-31 Christophe Viret, Aurore Rozières, Mathias Faure
NDP52/CALCOCO2 makes multiple contributions to selective autophagy. By interacting with cargos and LC3, NDP52 directs autophagy targets to autophagosomes. In addition, NDP52 promotes autophagosomes fusion with endolysosomes by connecting autophagosomes to MYOSIN VI. Recent studies reveal that Rab35 GTPase controls NDP52 recruitment to its targets and that NDP52 triggers MYOSIN VI (MYO6) motility.
Microvascular Mural Cell Organotypic Heterogeneity and Functional Plasticity Trends Cell Biol. (IF 15.333) Pub Date : 2018-01-05 Annegret Holm, Tina Heumann, Hellmut G. Augustin
Microvascular mural cells (MMCs), comprising pericytes and microvascular smooth muscle cells, are of increasing interest in multiple fields of research for their plasticity and their organotypic functional roles in microvascular homeostasis and disease. They have been described as a heterogeneous cell population constituting a continuum of cell phenotypes along the microvascular bed with vascular smooth muscle cells (VSMCs) at one end of the spectrum and pericytes at the other end. MMC organotypic subpopulations have been suggested to function in a tissue-context-dependent manner, thereby contributing to organ-specific functional roles. However, the phenotypic and organotypic heterogeneity as well as their origin and marker identification are hitherto poorly defined. Here we review recent work and emerging concepts regarding MMC phenotypic and organotypic heterogeneity and their functional plasticity in health and disease.
Increasing Diversity of Biological Membrane Fission Mechanisms Trends Cell Biol. (IF 15.333) Pub Date : 2018-01-04 Henri-François Renard, Ludger Johannes, Pierre Morsomme
Membrane fission is essential to life. It is required for many fundamental cellular processes, as diverse as cyto- and karyokinesis, organelle division, membrane repair, and membrane trafficking and endocytosis. While membrane fission was originally seen as resulting from the action of mechanoenzymes such as dynamin, it is clear that the reality is more complex. In this review, we propose an updated overview of fission mechanisms, and try to extract essential requirements for each. We also present examples of cellular processes that involve these fission mechanisms. Finally, we list pending questions, whether they are specific to a peculiar fission mechanism or more general to the field.
Notching a New Pathway in Vascular Flow Sensing Trends Cell Biol. (IF 15.333) Pub Date : 2018-01-02 Anne K. Lagendijk, Alpha S. Yap, Benjamin M. Hogan
Vascular barrier function is controlled at cell–cell junctions in response to blood flow, but how vascular endothelial cells sense and respond to flow remains to be understood. A recent study describes a flow-sensing pathway involving non-canonical Notch and cadherin signaling that sheds new light on mechanisms controlling the endothelial barrier.
Long Noncoding RNA in Cancer: Wiring Signaling Circuitry Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-20 Chunru Lin, Liuqing Yang
Long noncoding RNAs (lncRNAs), which are encoded by a vast less explored region of the human genome, may hold missing drivers of cancer and have gained attention recently as a potentially crucial layer of cancer cell regulation. lncRNAs are aberrantly expressed in a broad spectrum of cancers, and they play key roles in promoting and maintaining tumor initiation and progression, demonstrating their clinical potential as biomarkers and therapeutic targets. Recent discoveries have revealed that lncRNAs act as key signal transduction mediators in cancer signaling pathways by interacting with proteins, RNA, and lipids. Here, we review the mechanisms by which lncRNAs regulate cellular responses to extracellular signals and discuss their clinical potential as diagnostic indicators, stratification markers, and therapeutic targets of combinatorial treatments.
RANKL and RANK: From Mammalian Physiology to Cancer Treatment Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-11 Shuan Rao, Shane J.F. Cronin, Verena Sigl, Josef M. Penninger
The tumor necrosis factor (TNF) receptor RANK (TNFRSF11A) and its ligand RANKL (TNFSF11) regulate osteoclast development and bone metabolism. They also control stem cell expansion and proliferation of mammary epithelial cells via the sex hormone progesterone. As such, RANKL and RANK have been implicated in the onset of hormone-induced breast cancer. Recently, RANK/RANKL were identified as crucial regulators for BRCA1 mutation-driven breast cancer. Current prevention strategies for BRCA1 mutation carriers are associated with wide-ranging risks; therefore, the search for alternative, non-invasive strategies is of paramount importance. We summarize here the functions of the RANKL/RANK pathway in mammalian physiology and focus on its recently uncovered role in breast cancer. We propose that anti-RANKL therapy should be pursued as a preventative strategy for breast cancer.
Mechanisms of Carrier Formation during Clathrin-Independent Endocytosis Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-11 Antonio P.A. Ferreira, Emmanuel Boucrot
Clathrin-independent endocytosis (CIE) mediates the cellular uptake of many extracellular ligands, receptors, and pathogens, including several life-threatening bacterial toxins and viruses. So far, our understanding of CIE carrier formation has lagged behind that of clathrin-coated vesicles. Impediments have been the imprecise definition of some CIE pathways, the lack of specific cargoes being transported and of exclusive cytosolic markers and regulators. Notwithstanding these limitations, three distinct molecular mechanisms by which CIE carriers form can be defined. Cargo capture by cytosolic proteins is the main mechanism used by fast endophilin-mediated endocytosis (FEME) and interleukin 2 receptor (IL-2R) endocytosis. Acute signaling-induced membrane remodeling drives macropinocytosis. Finally, extracellular lipid or cargo clustering by the glycolipid-lectin (GL-Lect) hypothesis mediates the uptake of Shiga and cholera toxins and receptors by the CLIC/GEEC pathway. Here, we review these mechanisms and highlight current gaps in knowledge that will need to be addressed to complete our understanding of CIE.
Exploiting Metabolic Vulnerabilities of Cancer with Precision and Accuracy Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-08 Adam J. Wolpaw, Chi V. Dang
Links between oncogenic drivers and cancer cell metabolism have emerged over the past several decades, indicating that constitutive oncogenic growth signaling can render cancers susceptible to metabolic interventions. While significant progress has been achieved in the identification of metabolic vulnerabilities of cancer cells, the complexity of the tumor microenvironment (TME) and the dynamic nature of organismal circadian metabolism challenge the precision of targeting cancer metabolism. Here current progress in the areas of cancer metabolism and TME metabolism is reviewed, highlighting how cancer metabolism can be accurately and precisely targeted.
Fighting Resilient Cancers with Iron Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-07 Jonathan J. Chen, Lorenzo Galluzzi
Tumor progression and resistance to treatment are often accompanied by the polarization of malignant cells towards a mesenchymal or poorly differentiated state. Such a transition generates an accrued vulnerability to the induction of ferroptosis, potentially paving the way to novel therapeutic strategies for targeting residual disease in patients with cancer.
Epigenome in Early Mammalian Development: Inheritance, Reprogramming and Establishment Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-05 Qianhua Xu, Wei Xie
Drastic epigenetic reprogramming takes place during preimplantation development, leading to the conversion of terminally differentiated gametes to a totipotent embryo. Deficiencies in remodeling of the epigenomes can cause severe developmental defects, including embryonic lethality. However, how chromatin modifications and chromatin organization are reprogrammed upon fertilization in mammals has long remained elusive. Here, we review recent progress in understanding how the epigenome is dynamically regulated during early mammalian development. The latest studies, including many from genome-wide perspectives, have revealed unusual principles of reprogramming for histone modifications, chromatin accessibility, and 3D chromatin architecture. These advances have shed light on the regulatory network controlling the earliest development and maternal-zygotic transition.
Vms1: A Cytosolic CAT-Tailing Antagonist to Protect Mitochondria Trends Cell Biol. (IF 15.333) Pub Date : 2017-12-01 Stefan G. Kreft, Elke Deuerling
In eukaryotes, a cytosolic ribosome quality control complex recycles erroneously stalled ribosomes and modifies faulty nascent chains by ubiquitination and by C-terminal Ala- and Thr-extension (CAT-tailing). Reported recently in Cell, Izawa et al. identify cytosolic Vms1 (VCP/Cdc48-associated mitochondrial stress-responsive 1) as an inhibitor of CAT-tailing, which prevents mitochondrial dysfunction caused by imported CAT-tailed polypeptides.
Some contents have been Reproduced by permission of The Royal Society of Chemistry.
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