Programmed Cell Death 50 (And Beyond)
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Classification of Cell Death
Cell Death and Differentiation (2005) 12, 1463–1467 & 2005 Nature Publishing Group All rights reserved 1350-9047/05 $30.00 www.nature.com/cdd News and Commentary Classification of cell death: recommendations of the Nomenclature Committee on Cell Death G Kroemer*,1, WS El-Deiry2, P Golstein3, ME Peter4, D Vaux5, with or without, caspase activation and that ‘autophagic cell P Vandenabeele6, B Zhivotovsky7, MV Blagosklonny8, death’ represents a type of cell death with (but not necessarily W Malorni9, RA Knight10, M Piacentini11, S Nagata12 and through) autophagic vacuolization. This article details the G Melino10,13 2005 recommendations of NCCD. Over time, molecular definitions are expected to emerge for those forms of cell 1 CNRS-UMR8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, death that remain descriptive. F-94805 Villejuif, France 2 University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA Preface 3 Centre d’Immunologie INSERM/CNRS/Universite de la Mediterranee de Marseille-Luminy, Case 906, Avenue de Luminy, 13288 Marseille Cedex 9, It is obvious that clear definitions of objects that are only France shadows in Plato’s cage are difficult to be achieved. Cell death 4 The Ben May Institute for Cancer Research, University of Chicago, 924 E 57th and the different subroutines leading to cell death do not Street, Chicago, IL 60637, USA 5 escape this rule. Even worse, the notion of death is strongly Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, influenced by religious and cultural beliefs, which may UK 6 Molecular Signalling and Cell Death Unit, Department for Molecular Biomedical subliminally influence the scientific view of cell death. -
Meet the Gilded Lady 2 Mummies Now Open
Member Magazine Spring 2017 Vol. 42 No. 2 Mummies meet the gilded lady 2 mummies now open Seeing Inside Today, computerized inside of mummies, revealing CT scans of the Gilded Lady tomography (CT) scanning details about the person’s reveal that she was probably offers researchers glimpses age, appearance, and health. in her forties. They also suggest of mummified individuals “Scans like these are noninvasive, that she may have suffered like never before. By combining they’re repeatable, and they from tuberculosis, a common thousands of cross-sectioned can be done without damaging disease at the time. x-ray images, CT scans let the history that we’re trying researchers examine the to understand,” Thomas says. Mummy #30007, known as the Gilded Lady, is one of the most beautifully preserved mummies from The Field Museum’s collection, and one of 19 now on view in the special exhibition Mummies. For decades, keeping mummies like this one well preserved also meant severely limiting the ability of researchers to study them. The result is that little was known about the Gilded Lady beyond what could be gleaned from the mummy’s exterior, with its intricate linen bindings, gilded headdress, and painted facial features. Exterior details do offer some clues. The mummy dates from 30 BC–AD 395, a period when Egypt was a province of the Roman Empire. While the practice of mummification endured in Egypt, it was being transformed by Roman influences. Before the Roman era, for example, mummies had been placed in wooden coffins, while the Gilded Lady is preserved in only linen wrappings and cartonnage, a papier mâché-like material. -
Place Names Describing Fossils in Oral Traditions
Place names describing fossils in oral traditions ADRIENNE MAYOR Classics Department, Stanford University, Stanford CA 94305 (e-mail: [email protected]) Abstract: Folk explanations of notable geological features, including fossils, are found around the world. Observations of fossil exposures (bones, footprints, etc.) led to place names for rivers, mountains, valleys, mounds, caves, springs, tracks, and other geological and palaeonto- logical sites. Some names describe prehistoric remains and/or refer to traditional interpretations of fossils. This paper presents case studies of fossil-related place names in ancient and modern Europe and China, and Native American examples in Canada, the United States, and Mexico. Evidence for the earliest known fossil-related place names comes from ancient Greco-Roman and Chinese literature. The earliest documented fossil-related place name in the New World was preserved in a written text by the Spanish in the sixteenth century. In many instances, fossil geonames are purely descriptive; in others, however, the mythology about a specific fossil locality survives along with the name; in still other cases the geomythology is suggested by recorded traditions about similar palaeontological phenomena. The antiquity and continuity of some fossil-related place names shows that people had observed and speculated about miner- alized traces of extinct life forms long before modern scientific investigations. Traditional place names can reveal heretofore unknown geomyths as well as new geologically-important sites. Traditional folk names for geological features in the Named fossil sites in classical antiquity landscape commonly refer to mythological or and modern Greece legendary stories that accounted for them (Vitaliano 1973). Landmarks notable for conspicuous fossils Evidence for the practice of naming specific fossil have been named descriptively or mythologically locales can be found in classical antiquity. -
The Nature of Programmed Cell Death
Biological Theory https://doi.org/10.1007/s13752-018-0311-0 ORIGINAL ARTICLE The Nature of Programmed Cell Death Pierre M. Durand1 · Grant Ramsey2 Received: 14 March 2018 / Accepted: 10 October 2018 © Konrad Lorenz Institute for Evolution and Cognition Research 2018 Abstract In multicellular organisms, cells are frequently programmed to die. This makes good sense: cells that fail to, or are no longer playing important roles are eliminated. From the cell’s perspective, this also makes sense, since somatic cells in multicel- lular organisms require the cooperation of clonal relatives. In unicellular organisms, however, programmed cell death (PCD) poses a difficult and unresolved evolutionary problem. The empirical evidence for PCD in diverse microbial taxa has spurred debates about what precisely PCD means in the case of unicellular organisms (how it should be defined). In this article, we survey the concepts of PCD in the literature and the selective pressures associated with its evolution. We show that defini- tions of PCD have been almost entirely mechanistic and fail to separate questions concerning what PCD fundamentally is from questions about the kinds of mechanisms that realize PCD. We conclude that an evolutionary definition is best able to distinguish PCD from closely related phenomena. Specifically, we define “true” PCD as an adaptation for death triggered by abiotic or biotic environmental stresses. True PCD is thus not only an evolutionary product but must also have been a target of selection. Apparent PCD resulting from pleiotropy, genetic drift, or trade-offs is not true PCD. We call this “ersatz PCD.” Keywords Adaptation · Aging · Apoptosis · Price equation · Programmed cell death · Selection · Unicellular organisms Introduction in animal ontogeny, was made explicit several decades later (Glücksmann 1951; Lockshin and Williams 1964). -
The Biochemistry of Cell Death Cell Death: Apoptosis and Other Means to an End, Second Edition by Douglas R
Zampieri et al. Cell Death and Disease (2020) 11:259 https://doi.org/10.1038/s41419-020-2465-5 Cell Death & Disease BOOK REVIEW Open Access The biochemistry of cell death Cell Death: Apoptosis and Other Means to an End, Second Edition by Douglas R. Green, St. Jude Children’s Research Hospital, Cold Spring Harbor Laboratory Press, New York, 2018 Carlotta Zampieri 1, Carlo Ganini 1 and Gerry Melino 1 Can we impress you with a mind-blowing revelation? Douglas Green is one of the worldwide leading experts “Cells are not eternal in our bodies, but rather they on apoptosis and cell death. He has dealt with the role of encounter death!”1. cell death in the regulation of cancer and immune If someone pronounces this sentence at a biology class, response, studying the molecular events that drive the students will laugh. Why? Because cell death has been process, focusing on the induction-activation of apoptosis studied since the 60s of the last century. When we speak in T cells and the role of Myc, death receptors and Bcl-2 about apoptosis nowadays, we regard it as a well-known in this context. His deep understanding of the field truth. Anyway, this truth did not catch the attention of allowed him to write the first edition of this book in a scientists until the 1980s, where the interest in the field clear and straightforward manner, enriched by extremely exploded, leading to a dramatic increase of publications. informative figures. His talent as a biologist, as well as a Cell death passed “from neglect to hysteria” in only a few communicator, has been condensed in this second edi- years, citing Martin Raff2, one of the founders of the field. -
Snapshot: BCL-2 Proteins J
SnapShot: BCL-2 Proteins J. Marie Hardwick and Richard J. Youle Johns Hopkins, Baltimore, MD 21205, USA and NIH/NINDS, Bethesda, MD 20892, USA 404 Cell 138, July 24, 2009 ©2009 Elsevier Inc. DOI 10.1016/j.cell.2009.07.003 See online version for legend and references. SnapShot: BCL-2 Proteins J. Marie Hardwick and Richard J. Youle Johns Hopkins, Baltimore, MD 21205, USA and NIH/NINDS, Bethesda, MD 20892, USA BCL-2 family proteins regulate apoptotic cell death. BCL-2 proteins localize to intracellular membranes such as endoplasmic reticulum and mitochondria, and some fam- ily members translocate from the cytoplasm to mitochondria following a cell death stimulus. The prototypical family member Bcl-2 was originally identified at chromo- some translocation breakpoints in human follicular lymphoma and was subsequently shown to promote tumorigenesis by inhibiting cell death rather than by promoting cell-cycle progression. BCL-2 family proteins have traditionally been classified according to their function and their BCL-2 homology (BH) motifs. The general categories include multidomain antiapoptotic proteins (BH1-BH4), multidomain proapoptotic proteins (BH1-BH3), and proapoptotic BH3-only proteins (see Table 1). In the traditional view, anti-death BCL-2 family members in healthy cells hold pro-death BCL-2 family members in check. Upon receiving a death stimulus, BH3-only proteins inactivate the protective BCL-2 proteins, forcing them to release their pro-death partners. These pro-death BCL-2 family proteins homo-oligomerize to create pores in the mitochondrial outer membrane, resulting in cytochrome c release into the cytoplasm, which leads to caspase activation and cell death. -
Viruses and the Origin of Microbiome Selection and Immunity
The ISME Journal (2017) 11, 835–840 © 2017 International Society for Microbial Ecology All rights reserved 1751-7362/17 www.nature.com/ismej PERSPECTIVE Viruses and the origin of microbiome selection and immunity Steven D Quistad1,2,3, Juris A Grasis1, Jeremy J Barr1,4 and Forest L Rohwer1 1Department of Biology, San Diego State University, San Diego, CA, USA; 2Laboratoire de Colloïdes et Matériaux Divisés (LCMD), Institute of Chemistry, Biology, and Innovation, ESPCI ParisTech/CNRS UMR 8231/PSL Research University, Paris, France; 3Laboratoire de Colloïdes et Matériaux Divisés (LCMD), Institute of Chemistry, Biology, and Innovation, ESPCI ParisTech/CNRS UMR 8231/PSL Research University, Paris, France and 4School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia The last common metazoan ancestor (LCMA) emerged over half a billion years ago. These complex metazoans provided newly available niche space for viruses and microbes. Modern day contemporaries, such as cnidarians, suggest that the LCMA consisted of two cell layers: a basal endoderm and a mucus-secreting ectoderm, which formed a surface mucus layer (SML). Here we propose a model for the origin of metazoan immunity based on external and internal microbial selection mechanisms. In this model, the SML concentrated bacteria and their associated viruses (phage) through physical dynamics (that is, the slower flow fields near a diffusive boundary layer), which selected for mucin-binding capabilities. The concentration of phage within the SML provided the LCMA with an external microbial selective described by the bacteriophage adherence to mucus (BAM) model. In the BAM model, phage adhere to mucus protecting the metazoan host against invading, potentially pathogenic bacteria. -
Issue of the FOSSIL
Official Publication of The Fossils, The Historians of Amateur Journalism The Fossil Volume 116, No. 3, Whole No. 383 Sunnyvale, California April 2020 Fossil Profile My Ajay Mentors by Linda Donaldson FOSSIL EDITOR Dave Tribby has asked me to provide a the beginning of a long love affair. It was almost the few thoughts on my friends and mentors in the world last press I saw exit my door. of amateur journalism. Though I’m not active now, He also introduced me to ajayers in my hometown thanks mostly to vision problems that make it hard to of Portsmouth, Ohio: Karl X. Williams and Charlie read the bundles, I was fortunate Phillips. The two of them were to have had several good men happy to share or sell me some of tors. I am still a Fossil—it’s hard their treasure troves of type or to totally desert the realm. necessary equipment. Much has It started with the one and been written of Karl, a Lone only J. Hill Hamon, whom I met Scout young printer in the 1920s, as my Biology professor at AAPA founding father, and a Transylvania University in Lex Fossil. To this day I possess a pa ington, Kentucky in January of per cutter I bought from Katie, 1972. I didn’t start learning the Karl’s widow. I was employed printing part until a short term about five years as a rubber class in December of 1972. He set stamp maker by Karl’s daughter out lots of old type on the Bio Pam and soninlaw Gary. -
Dual Effects of Thyroid Hormone on Neurons and Neurogenesis
Lin et al. Cell Death and Disease (2020) 11:671 https://doi.org/10.1038/s41419-020-02836-9 Cell Death & Disease ARTICLE Open Access Dual effects of thyroid hormone on neurons and neurogenesis in traumatic brain injury Chao Lin1,2, Nan Li3, Hanxiao Chang1,2,Yuqishen1,2,ZhengLi1,2,Wuwei1,2,HuaChen1,2,HuaLu1,2,JingJi 1,2 and Ning Liu1,2 Abstract Thyroid hormone (TH) plays a crucial role in neurodevelopment, but its function and specific mechanisms remain unclear after traumatic brain injury (TBI). Here we found that treatment with triiodothyronine (T3) ameliorated the progression of neurological deficits in mice subjected to TBI. The data showed that T3 reduced neural death and promoted the elimination of damaged mitochondria via mitophagy. However, T3 did not prevent TBI-induced cell death in phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (Pink1) knockout mice suggesting the involvement of mitophagy. Moreover, we also found that T3 promoted neurogenesis via crosstalk between mature neurons and neural stem cells (NSCs) after TBI. In neuron cultures undergoing oxygen and glucose deprivation (OGD), conditioned neuron culture medium collected after T3 treatment enhanced the in vitro differentiation of NSCs into mature neurons, a process in which mitophagy was required. Taken together, these data suggested that T3 treatment could provide a therapeutic approach for TBI by preventing neuronal death via mitophagy and promoting neurogenesis via neuron–NSC crosstalk. 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; Introduction treatments focus only on preventing complications or Traumatic brain injury (TBI) is considered to be a providing support in nature. leading cause of substantial mortality and long-term dis- Thyroid hormone (TH) is crucial for neural stem cell ability among young adults worldwide1. -
Sonic Hedgehog a Neural Tube Anti-Apoptotic Factor 4013 Other Side of the Neural Plate, Remaining in Contact with Midline Cells, RESULTS Was Used As a Control
Development 128, 4011-4020 (2001) 4011 Printed in Great Britain © The Company of Biologists Limited 2001 DEV2740 Anti-apoptotic role of Sonic hedgehog protein at the early stages of nervous system organogenesis Jean-Baptiste Charrier, Françoise Lapointe, Nicole M. Le Douarin and Marie-Aimée Teillet* Institut d’Embryologie Cellulaire et Moléculaire, CNRS FRE2160, 49bis Avenue de la Belle Gabrielle, 94736 Nogent-sur-Marne Cedex, France *Author for correspondence (e-mail: [email protected]) Accepted 19 July 2001 SUMMARY In vertebrates the neural tube, like most of the embryonic notochord or a floor plate fragment in its vicinity. The organs, shows discreet areas of programmed cell death at neural tube can also be recovered by transplanting it into several stages during development. In the chick embryo, a stage-matched chick embryo having one of these cell death is dramatically increased in the developing structures. In addition, cells engineered to produce Sonic nervous system and other tissues when the midline cells, hedgehog protein (SHH) can mimic the effect of the notochord and floor plate, are prevented from forming by notochord and floor plate cells in in situ grafts and excision of the axial-paraxial hinge (APH), i.e. caudal transplantation experiments. SHH can thus counteract a Hensen’s node and rostral primitive streak, at the 6-somite built-in cell death program and thereby contribute to organ stage (Charrier, J. B., Teillet, M.-A., Lapointe, F. and Le morphogenesis, in particular in the central nervous system. Douarin, N. M. (1999). Development 126, 4771-4783). In this paper we demonstrate that one day after APH excision, Key words: Apoptosis, Avian embryo, Cell death, Cell survival, when dramatic apoptosis is already present in the neural Floor plate, Notochord, Quail/chick, Shh, Somite, Neural tube, tube, the latter can be rescued from death by grafting a Spinal cord INTRODUCTION generally induces an inflammatory response. -
The Carbon Cycle
The Carbon Cycle Overview of the Carbon Cycle The movement of carbon from one area to another is the basis for the carbon cycle. Carbon is important for all life on Earth. All living things are made up of carbon. Carbon is produced by both natural and human-made (anthropogenic) sources. Carbon Cycle Page 1 Nature’s Carbon Sources Carbon is found in the Carbon is found in the lithosphere Carbon is found in the Carbon is found in the atmosphere mostly as carbon in the form of carbonate rocks. biosphere stored in plants and hydrosphere dissolved in ocean dioxide. Animal and plant Carbonate rocks came from trees. Plants use carbon dioxide water and lakes. respiration place carbon into ancient marine plankton that sunk from the atmosphere to make the atmosphere. When you to the bottom of the ocean the building blocks of food Carbon is used by many exhale, you are placing carbon hundreds of millions of years ago during photosynthesis. organisms to produce shells. dioxide into the atmosphere. that were then exposed to heat Marine plants use cabon for and pressure. photosynthesis. The organic matter that is produced Carbon is also found in fossil fuels, becomes food in the aquatic such as petroleum (crude oil), coal, ecosystem. and natural gas. Carbon is also found in soil from dead and decaying animals and animal waste. Carbon Cycle Page 2 Natural Carbon Releases into the Atmosphere Carbon is released into the atmosphere from both natural and man-made causes. Here are examples to how nature places carbon into the atmosphere. -
Mechanisms of Programmed Cell Death in the Developing Brain
_TINS July 2000 [final corr.] 12/6/00 10:39 am Page 291 R EVIEW Mechanisms of programmed cell death in the developing brain Chia-Yi Kuan, Kevin A. Roth, Richard A. Flavell and Pasko Rakic Programmed cell death (apoptosis) is an important mechanism that determines the size and shape of the vertebrate nervous system. Recent gene-targeting studies have indicated that homologs of the cell-death pathway in the nematode Caenorhabditis elegans have analogous functions in apoptosis in the developing mammalian brain.However,epistatic genetic analysis has revealed that the apoptosis of progenitor cells during early embryonic development and apoptosis of postmitotic neurons at later stage of brain development have distinct roles and mechanisms.These results provide new insight on the significance and mechanism of neural cell death in mammalian brain development. Trends Neurosci. (2000) 23, 291–297 ELL DEATH has long been recognized to occur in homologs of ced-3 comprise a family of cysteine- Cmost neuronal populations during normal devel- containing, aspartate-specific proteases called caspases5. opment of the vertebrate nervous system (reviewed in The ced-4 homolog is identified as one of the apoptosis Ref. 1). Traditionally, the investigation of neural death protease-activating factors (APAFs)6. The mammalian in development focused on the role of target-derived homologs of ced-9 belong to a growing family of Bcl2 survival factors such as NGF and related neurotrophins proteins, which share the Bcl2-homology (BH) domain (see Ref. 2 for a review). However, in the past few years, and are either pro- or anti-apoptotic7. The cloning of the genetic analysis of programmed cell death in the egl-1 indicates that it is similar to the BH3-domain- nematode Caenorhabditis elegans has inspired new ap- containing, pro-apoptotic subfamily of Bcl2 proteins4.