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- Volume 22, 2006
Annual Review of Cell and Developmental Biology - Volume 22, 2006
Volume 22, 2006
- Preface
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From Nuclear Transfer to Nuclear Reprogramming: The Reversal of Cell Differentiation
Vol. 22 (2006), pp. 1–22More LessThis is a personal historical account of events leading from the earliest success in vertebrate nuclear transfer to the current hope that nuclear reprogramming may facilitate cell replacement therapy. Early morphological evidence in Amphibia for the toti- or multipotentiality of some nuclei from differentiated cells first established the principle of the conservation of the genome during cell differentiation. Molecular markers show that many somatic cell nuclei are reprogrammed to an embryonic pattern of gene expression soon after nuclear transplantation to eggs. The germinal vesicles of oocytes in first meiotic prophase have a direct reprogramming activity on mammalian as well as amphibian nuclei and offer a route to identify nuclear reprogramming molecules. Amphibian eggs and oocytes have a truly remarkable ability to transcribe genes as DNA or nuclei, to translate mRNA, and to modify or localize proteins injected into them. The development of nuclear transplant embryos depends on the ability of cells to interpret small concentration changes of signal factors in the community effect and in morphogen gradients. Many difficulties in a career can be overcome by analyzing in increasing depth the same fundamentally interesting and important problem.
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How Does Voltage Open an Ion Channel?
Vol. 22 (2006), pp. 23–52More LessAbstractNeurons transmit information through electrical signals generated by voltage-gated ion channels. These channels consist of a large superfamily of proteins that form channels selective for potassium, sodium, or calcium ions. In this review we focus on the molecular mechanisms by which these channels convert changes in membrane voltage into the opening and closing of “gates” that turn ion conductance on and off. An explosion of new studies in the last year, including the first X-ray crystal structure of a mammalian voltage-gated potassium channel, has led to radically different interpretations of the structure and molecular motion of the voltage sensor. The interpretations are as distinct as the techniques employed for the studies: crystallography, fluorescence, accessibility analysis, and electrophysiology. We discuss the likely causes of the discrepant results in an attempt to identify the missing information that will help resolve the controversy and reveal the mechanism by which a voltage sensor controls the channel's gates.
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Cellulose Synthesis in Higher Plants
Vol. 22 (2006), pp. 53–78More LessAbstractCellulose microfibrils play essential roles in the organization of plant cell walls, thereby allowing a growth habit based on turgor. The fibrils are made by 30 nm diameter plasma membrane complexes composed of approximately 36 subunits representing at least three types of related CESA proteins. The complexes assemble in the Golgi, where they are inactive, and move to the plasma membrane, where they become activated. The complexes move through the plasma membrane during cellulose synthesis in directions that coincide with the orientation of microtubules. Recent, simultaneous, live-cell imaging of cellulose synthase and microtubules indicates that the microtubules exert a direct influence on the orientation of cellulose deposition. Genetic studies in Arabidopsis have identified a number of genes that contribute to the overall process of cellulose synthesis, but the role of these proteins is not yet known.
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Mitochondrial Fusion and Fission in Mammals
Vol. 22 (2006), pp. 79–99More LessAbstractEukaryotic cells maintain the overall shape of their mitochondria by balancing the opposing processes of mitochondrial fusion and fission. Unbalanced fission leads to mitochondrial fragmentation, and unbalanced fusion leads to mitochondrial elongation. Moreover, these processes control not only the shape but also the function of mitochondria. Mitochondrial dynamics allows mitochondria to interact with each other; without such dynamics, the mitochondrial population consists of autonomous organelles that have impaired function. Key components of the mitochondrial fusion and fission machinery have been identified, allowing initial dissection of their mechanisms of action. These components play important roles in mitochondrial function and development as well as programmed cell death. Disruption of the fusion machinery leads to neurodegenerative disease.
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Agrobacterium tumefaciens and Plant Cell Interactions and Activities Required for Interkingdom Macromolecular Transfer
Vol. 22 (2006), pp. 101–127More LessAbstractHost recognition and macromolecular transfer of virulence-mediating effectors represent critical steps in the successful transformation of plant cells by Agrobacterium tumefaciens. This review focuses on bacterial and plant-encoded components that interact to mediate these two processes. First, we examine the means by which Agrobacterium recognizes the host, via both diffusible plant-derived chemicals and cell-cell contact, with emphasis on the mechanisms by which multiple host signals are recognized and activate the virulence process. Second, we characterize the recognition and transfer of protein and protein-DNA complexes through the bacterial and plant cell membrane and wall barriers, emphasizing the central role of a type IV secretion system—the VirB complex—in this process.
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Cholesterol Sensing, Trafficking, and Esterification
Vol. 22 (2006), pp. 129–157More LessAbstractMammalian cells acquire cholesterol from low-density lipoprotein (LDL) and from endogenous biosynthesis. The roles of the Niemann-Pick type C1 protein in mediating the endosomal transport of LDL-derived cholesterol and endogenously synthesized cholesterol are discussed. Excess cellular cholesterol is converted to cholesteryl esters by the enzyme acyl-coenzyme A:cholesterol acyltransferase (ACAT) 1 or is removed from a cell by cellular cholesterol efflux at the plasma membrane. A close relationship between the ACAT substrate pool and the cholesterol efflux pool is proposed. Sterol-sensing domains (SSDs) are present in several membrane proteins, including NPC1, HMG-CoA reductase, and the SREBP cleavage–activating protein. The functions of SSDs are described. ACAT1 is an endoplasmic reticulum cholesterol sensor and contains a signature motif characteristic of the membrane-bound acyltransferase family. The nonvesicular cholesterol translocation processes involve the START domain proteins and the oxysterol binding protein–related proteins (ORPs). The properties of these proteins are summarized.
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Modification of Proteins by Ubiquitin and Ubiquitin-Like Proteins
Vol. 22 (2006), pp. 159–180More LessAbstractFollowing the discovery of protein modification by the small, highly conserved ubiquitin polypeptide, a number of distinct ubiquitin-like proteins (Ubls) have been found to function as protein modifiers as well. These Ubls, which include SUMO, ISG15, Nedd8, and Atg8, function as critical regulators of many cellular processes, including transcription, DNA repair, signal transduction, autophagy, and cell-cycle control. A growing body of data also implicates the dysregulation of Ubl-substrate modification and mutations in the Ubl-conjugation machinery in the etiology and progression of a number of human diseases. The primary aim of this review is to summarize the latest developments in our understanding of the different Ubl-protein modification systems, including the shared and unique features of these related pathways.
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Endocytosis, Endosome Trafficking, and the Regulation of Drosophila Development
Vol. 22 (2006), pp. 181–206More LessAbstractEndocytosis and endosome trafficking regulate cell signaling in unexpected ways. Here we review the contribution that Drosophila research has made to this exciting field. In addition to attenuating signaling, endocytosis shapes morphogen gradients, activates ligands, and regulates spatially receptor activation within a single cell. Moreover, some receptors signal from within endosomes, and the ability of a specific type of endosome to form controls the ability of cells to signal. Experiments in Drosophila reveal that through regulation of a variety of cell signaling pathways, endocytosis controls cell patterning and cell fate.
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Tight Junctions and Cell Polarity
Vol. 22 (2006), pp. 207–235More LessAbstractThe tight junction is an intracellular junctional structure that mediates adhesion between epithelial cells and is required for epithelial cell function. Tight junctions control paracellular permeability across epithelial cell sheets and also serve as a barrier to intramembrane diffusion of components between a cell's apical and basolateral membrane domains. Recent genetic and biochemical studies in invertebrates and vertebrates indicate that tight junction proteins play an important role in the establishment and maintenance of apico-basal polarity. Proteins involved in epithelial cell polarization form evolutionarily conserved multiprotein complexes at the tight junction, and these protein complexes regulate the architecture of epithelia throughout the polarization process. Accumulating information regarding the regulation of these polarity proteins will lead to a better understanding of the molecular mechanisms whereby cell polarity is established.
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In Vivo Migration: A Germ Cell Perspective
Vol. 22 (2006), pp. 237–265More LessAbstractThe basic concepts of the molecular machinery that mediates cell migration have been gleaned from cell culture systems. However, the three-dimensional environment within an organism presents migrating cells with a much greater challenge. They must move between and among other cells while interpreting multiple attractive and repulsive cues to choose their proper path. They must coordinate their cell adhesion with their surroundings and know when to start and stop moving. New insights into the control of these remaining mysteries have emerged from genetic dissection and live imaging of germ cell migration in Drosophila, zebrafish, and mouse embryos. In this review, we first describe germ cell migration in cellular and mechanistic detail in these different model systems. We then compare these systems to highlight the emerging principles. Finally, we contrast the migration of germ cells with that of immune and cancer cells to outline the conserved and different mechanisms.
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Neural Crest Stem and Progenitor Cells
Vol. 22 (2006), pp. 267–286More LessAbstractNeural crest cells are a multipotent, migratory cell population that generates an astonishingly diverse array of cell types during vertebrate development. These include bones; tendons; neurons; glia; melanocytes; and connective, endocrine, and adipose tissue. With a limited capacity for self-renewal and a wide range of differentiation fates, neural crest cells bear many of the hallmarks of stem cells and persist throughout embryonic and adult development. But are all neural crest cells true stem cells, or do the majority of neural crest cells more closely resemble progenitor cells? In this review we discuss recent advances in characterizing the properties of neural crest cells, together with their potential for tissue-specific repair.
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Of Extracellular Matrix, Scaffolds, and Signaling: Tissue Architecture Regulates Development, Homeostasis, and Cancer
Vol. 22 (2006), pp. 287–309More LessAbstractThe microenvironment influences gene expression so that the behavior of a cell is largely determined by its interactions with the extracellular matrix, neighboring cells, and soluble local and systemic cues. We describe the essential roles of context and organ structure in directing mammary gland development and differentiated function and in determining the response to oncogenic insults, including mutations. We expand on the concept of “dynamic reciprocity” to present an integrated view of development, cancer, and aging and posit that genes are like the keys on a piano: Although they are essential, it is the context that makes the music.
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Intrinsic Regulators of Pancreatic β-Cell Proliferation
Vol. 22 (2006), pp. 311–338More LessAbstractOnce thought incapable of significant proliferation, the pancreatic β-cell has recently been shown to harbor immense powers of self-renewal. Pancreatic β-cells, the sole source of insulin in vertebrate animals, can grow facultatively to a degree unmatched by other organs in experimental animals. β-cell growth matches changes in systemic insulin demand, which increase during common physiologic states such as aging, obesity, and pregnancy. Compensatory changes in β-cell mass are controlled by β-cell proliferation. Here we review recent advances in our understanding of the intrinsic factors and mechanisms that control β-cell cycle progression. Dysregulation of β-cell proliferation is emerging as a fundamental feature in the pathogenesis of human disease states such as cancer and diabetes mellitus. New experimental observations and studies of these diseases suggest that β-cell fate and expansion are coordinately regulated. We speculate on how these advances may accelerate the discovery of new strategies for the treatment of diseases characterized by a deficiency or excess of β-cells.
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Epidermal Stem Cells of the Skin
Vol. 22 (2006), pp. 339–373More LessAbstractThe skin constantly renews itself throughout adult life, and the hair follicle undergoes a perpetual cycle of growth and degeneration. Stem cells (SCs) residing in the epidermis and hair follicle ensure the maintenance of adult skin homeostasis and hair regeneration, but they also participate in the repair of the epidermis after injuries. We summarize here the current knowledge of epidermal SCs of the adult skin. We discuss their fundamental characteristics, the methods recently designed to isolate these cells, the genes preferentially expressed in the multipotent SC niche, and the signaling pathways involved in SC niche formation, SC maintenance, and activation. Finally, we speculate on how the deregulation of these pathways may lead to cancer formation.
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The Molecular Diversity of Glycosaminoglycans Shapes Animal Development
Vol. 22 (2006), pp. 375–407More LessAbstractProteoglycans (PGs), molecules in which glycosaminoglycans (GAGs) are covalently linked to a protein core, are components of the extracellular matrix of all multicellular organisms. Sugar moieties in GAGs are often extensively modified, which make these molecules enormously complex. We discuss here the role of PGs during animal development, emphasizing the in vivo significance of sugar modifications. We explore a model in which the modification patterns of GAG chains may provide a specific code that contributes to the correct development of a multicellular organism.
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Recognition and Signaling by Toll-Like Receptors
Vol. 22 (2006), pp. 409–437More LessAbstractToll-like receptors (TLRs) are transmembrane proteins that detect invading pathogens by binding conserved, microbially derived molecules and that induce signaling cascades for proinflammatory gene expression. A critical component of the innate immune system, TLRs utilize leucine-rich-repeat motifs for ligand binding and a shared cytoplasmic domain to recruit the adaptors MyD88, TRIF, TIRAP, and/or TRAM for downstream signaling. Despite significant domain conservation, TLRs induce gene programs that lead not only to the robust production of general proinflammatory mediators but also to the production of unique effectors, which provide pathogen-tailored immune responses. Here we review the mechanisms by which TLRs recognize pathogens and induce distinct signaling cascades.
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The Formation of TGN-to-Plasma-Membrane Transport Carriers
Vol. 22 (2006), pp. 439–455More LessAbstractIn the trans-Golgi network (TGN), proteins are sorted for transport to the endosomes, plasma membrane, preceding Golgi cisternae, and endoplasmic reticulum. The formation of clathrin-coated vesicles for transport to the endosomes and of COP-I-coated vesicles for retrograde trafficking is fairly well characterized at the molecular level. We describe our current understanding of the TGN-to-cell-surface carriers, with a specific focus on the components involved in membrane fission. Inhibiting the fission machinery promotes growth of transport carriers into large tubules that remain attached to the TGN. Overactivating this machinery, on the other hand, vesiculates the TGN. To understand how membrane fission is regulated by cargo to form transport carriers yet prevents complete vesiculation of the TGN remains a daunting challenge. We discuss these issues with regard to TGN-to-cell-surface transport carriers.
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Iron-Sulfur Protein Biogenesis in Eukaryotes: Components and Mechanisms
Vol. 22 (2006), pp. 457–486More LessAbstractIron-sulfur (Fe/S) clusters require a complex set of proteins to become assembled and incorporated into apoproteins in a living cell. Researchers have described three distinct assembly systems in eukaryotes that are involved in the maturation of cellular Fe/S proteins. Mitochondria are central for biogenesis. They contain the ISC—the iron-sulfur cluster assembly machinery that was inherited from a similar system of eubacteria in evolution and is involved in biogenesis of all cellular Fe/S proteins. The basic principle of mitochondrial (and bacterial) Fe/S protein maturation is the synthesis of the Fe/S cluster on a scaffold protein before the cluster is transferred to apoproteins. Biogenesis of cytosolic and nuclear Fe/S proteins is facilitated by the cytosolic iron-sulfur protein assembly (CIA) apparatus. This process requires the participation of mitochondria that export a still unknown component via the ISC export machinery, including an ABC transporter.
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Intracellular Signaling by the Unfolded Protein Response
Vol. 22 (2006), pp. 487–508More LessAbstractThe unfolded protein response (UPR) is an intracellular signaling pathway that is activated by the accumulation of unfolded proteins in the endoplasmic reticulum (ER). UPR activation triggers an extensive transcriptional response, which adjusts the ER protein folding capacity according to need. As such, the UPR constitutes a paradigm of an intracellular control mechanism that adjusts organelle abundance in response to environmental or developmental clues. The pathway involves activation of ER unfolded protein sensors that operate in parallel circuitries to transmit information across the ER membrane, activating a set of downstream transcription factors by mechanisms that are unusual yet rudimentarily conserved in all eukaryotes. Recent results shed light on the mechanisms by which unfolded proteins are sensed in the ER and by which the unfolded protein signals are relayed and integrated to reestablish homeostasis in the cell's protein folding capacity or—if this cannot be achieved—commit cells to apoptosis.
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Previous Volumes
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Volume 40 (2024)
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Volume 39 (2023)
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Volume 38 (2022)
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Volume 37 (2021)
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Volume 36 (2020)
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Volume 35 (2019)
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Volume 34 (2018)
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Volume 33 (2017)
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Volume 32 (2016)
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Volume 31 (2015)
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Volume 30 (2014)
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Volume 29 (2013)
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Volume 28 (2012)
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Volume 27 (2011)
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Volume 26 (2010)
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Volume 25 (2009)
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Volume 24 (2008)
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Volume 23 (2007)
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Volume 22 (2006)
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Volume 21 (2005)
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Volume 20 (2004)
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Volume 19 (2003)
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Volume 18 (2002)
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Volume 17 (2001)
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Volume 16 (2000)
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Volume 15 (1999)
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Volume 14 (1998)
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Volume 13 (1997)
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Volume 12 (1996)
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Volume 11 (1995)
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Volume 10 (1994)
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Volume 9 (1993)
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Volume 8 (1992)
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Volume 7 (1991)
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Volume 6 (1990)
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Volume 5 (1989)
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Volume 4 (1988)
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Volume 3 (1987)
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Volume 2 (1986)
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Volume 1 (1985)
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Volume 0 (1932)