Rethinking Modern Theories of Ageing and Their Classification: the Proximate Mechanisms and the Ultimate Explanations

Total Page:16

File Type:pdf, Size:1020Kb

Rethinking Modern Theories of Ageing and Their Classification: the Proximate Mechanisms and the Ultimate Explanations Piotr Chmielewski Rethinking modern theories of ageing Anthropological Review • Vol. 80(3), 259–272 (2017) Rethinking modern theories of ageing and their classification: the proximate mechanisms and the ultimate explanations Piotr Chmielewski Division of Anatomy, Department of Human Morphology and Embryology, Faculty of Medicine, Wrocław Medical University, Poland ABSTRACT: For a very long time, ageing has been an insurmountable problem in biology. The collection of age-dependent changes that render ageing individuals progressively more likely to die seemed to be an in- tractable labyrinth of alterations and associations whose direct mechanisms and ultimate explanations were too complex and difficult to understand. The science of ageing has always been fraught with insuperable problems and obstacles. In 1990, Zhores Medvedev presented a list of roughly 300 different hypotheses to illustrate this remarkable complexity of the ageing process and various approaches to understanding its mechanisms, though none of these hypotheses or aspect theories could be the general theory of senescence. Moreover, in the light of current data some of these ideas are obsolete and inapplicable. Nonetheless, the misconception that there are hundreds of valid theories of ageing persists among many researchers and authors. In addition, some of these obsolete and discarded hypotheses, such as the rate of living theory, the wear and tear theory, the poisoning theory, or the entropy theory still can be found in today’s medical text- books, scientific publications aimed at the general public, and even in scientific writing. In fact, there are only several modern theories of ageing supported by compelling evidence that attempt to explain most of the data in current gerontology. These theories are competing to be a general and integrated model of ageing, making it unlikely that all of them could be true. This review summarises briefly several selected modern theories of senescence in the light of the contemporary knowledge of the biological basis for ageing and current data. KEY WORDS: ageing, gerontology, programmed ageing, quasi-programmed ageing, senescence, stochastic ageing, theories of ageing the ultimate explanations), thereby ad- Introduction dressing the question “Why did ageing evolve?” and those which concentrate on Traditionally, theories of biological age- proximate mechanisms, such as genes ing have been classified into two cat- and other molecular factors, that directly egories, i.e. those which explain the drive the ageing process (i.e. the proxi- evolutionary origin of senescence (i.e. mate explanations), thereby answering Review Article Received: July 4, 2017; Accepted for publication: August 10, 2017 DOI: 10.1515/anre-2017-0021 © 2017 Polish Anthropological Society 260 Piotr Chmielewski the question “How do we age?”. The longer current (Rattan 2006), this dual- first group of theories was divided into ism lingers on as it illustrates the core deterministic models that explain ageing of the long-running dispute among ger- as an atavistic, programmed, and altru- ontologists, which is known as the great istic process that is driven by hundreds conundrum in gerontology (cf. Kirkwood or thousands of genes and molecular and Melov 2011; Skulachev 2011; 2012; factors to purposefully eliminate older 2013). Interestingly, some authors sug- individuals from the population through gest that these two fiercely competing higher levels of natural selection, chief- theories “are not necessarily mutually ly group selection and evolvability at the exclusive” (Sergiev et al. 2015) as real population level (Skulachev 1997; Longo ageing can vary across species and the et al. 2005; Skulachev and Longo 2005), build-up of random molecular damage and stochastic models that explain age- or the decreased capacity for repair and ing as a completely passive and non-pro- maintenance of the body can be accelerat- grammed process that is driven by the ed by programmed aspects of senescence gradual accumulation of random molecu- whose traces and signalling pathways lar and cellular damage that is non-adap- become more and more evident thanks tive and not programmed since it is defi- to recent research into the genetics and nitely non-adaptive at the levels where epigenetics of ageing. natural selection takes place according to Unlike in the case of evolutionary the selfish gene theory (Kirkwood 2005). explanations or at least the milestones Some of the proponents of deter- (Weismann 1889; Medawar 1952; Wil- ministic models of ageing opine that liams 1957; Kirkwood 1977), a surpris- Dawkins’ theory is definitely specious, ingly large number of hypotheses related but some of these deterministic theories to the proximate mechanisms and aspects are based on flimsy argumentation (e.g. of ageing have been put forward. Indeed, entropy cannot be the real cause of age- ageing used to be an insurmountable ing, hence the theory of molecular entro- problem in biology for a long time (Holli- py is definitely invalid, while molecular day 2006; Hayflick 2007) since the collec- entropy is caused by the fact that living tion of age-dependent changes that ren- systems have built-in mechanisms that der ageing individuals progressively more actively resist entropy which tend to fal- likely to die seemed to be an intractable ter and fail in late ontogeny, and thus the labyrinth of alterations and associations causes of molecular entropy are of differ- whose direct mechanisms and ultimate ent nature) and highly speculative mod- explanations were too complex and diffi- els of the evolution of senescence such cult to follow. Thus, the science of ageing as group selection and evolvability. The has always been fraught with insuperable vast majority of researchers and scholars problems and obstacles. Edward Schnei- do not support such a view on the evolu- der, a distinguished American gerontolo- tion of senescence, which does not mean gist, quipped: “If you think that cancer is that it is utterly meaningless and without complicated, look at ageing”. Indeed, the some merit. ageing process is immensely complex and Although the above-mentioned cat- multifaceted. It is far more complex than egorization of theories of ageing into cancer. It was a Russian biogerontologist, programmed and stochastic models is no Zhores Medvedev (1990), who compiled Rethinking modern theories of ageing 261 a list of over 300 different hypotheses of general and integrated model of ageing, varying kinds to illustrate this remarka- making it unlikely that all of them could ble complexity of the ageing process and be true. This review summarises briefly various approaches to understanding its some of these modern theories of biolog- mechanisms, though none of these work- ical ageing in the light of new data and ing hypotheses or aspect theories could the contemporary knowledge of the bio- be labelled as the theory of ageing (Rat- logical basis for ageing. tan 2006). Moreover, some of them are now obsolete in the light of current data Programmed ageing: altruistic on the biological basis for ageing. Never- theless, the misconception that there are suicide through slow more than 300 valid theories of ageing “phenoptosis” or numerous valid theories and the sci- ence of ageing has not made any progress Ageing is arguably the most familiar as- since this list was presented still persists pect of ontogenetic development and among many authors and researchers. the latter process is tightly controlled In addition, some of these outdated and and programmed. Moreover, the ageing discarded hypotheses, such as the rate of process involves a predictable regulari- living theory proposed by Pearl, the early ty and reproducibility of age-dependent version of the wear and tear theory, Rub- changes in numerous morphological and ner’s theory, Mechnikov’s theory, the poi- physiological characteristics which occur soning theory, the entropy theory, and so with advancing age in all ageing individ- forth still can be found in today’s medical uals within a given species, which makes textbooks, scientific publications aimed at it rather improbable that all these altera- the general public, and scientific writing. tions depend on random, i.e. stochastic, In fact, there are only several modern factors. Therefore, since time immemo- theories of ageing supported by com- rial ageing has been perceived as pro- pelling evidence that attempt to explain grammed. This group of explanations is most of the data in current gerontolo- very old and extremely widespread, es- gy, including findings from the genetics pecially among non-specialists and new- and epigenetics of ageing and longevity, comers to the field of biogerontology. the underlying causes of sex differences It was August Weismann (1889) who in healthspan and lifespan, the effects first introduced the idea that a group of calorie restriction in animal models, of ageing and dying organisms would the effects of antioxidants on health have a fitness advantage over a group of and longevity, the mysterious effect of non-ageing and immortal organisms be- hormesis, and the links with age-related cause older, ill, and worn-out individuals diseases like cancer, cardiovascular dis- are not only valueless but also harmful to ease (CVD), and type 2 diabetes (for a the group from an evolutionary point of review, see Harman 2006; Rattan 2006; view. Therefore, although death was not Jin 2010; Sikora 2014; Kochman 2015; a primary necessity, it has become a sec- Lipsky and King 2015; Sergiev et al. ondarily
Recommended publications
  • Symposium on Aging June 19, 2015 Symposium on Aging the Paul F
    The 2015 Harvard / Paul F. Glenn Symposium on Aging June 19, 2015 Symposium on Aging The Paul F. Glenn Laboratories for the Biological Mechanisms of Aging Agenda 10th Anniversary Symposium Welcome to the 10th Annual Harvard/Paul F. Glenn Symposium on Aging. June 19, 2015 Each year, the Paul F. Glenn Laboratories host the Harvard Symposium 9:00 - 5:00 on Aging with a mission to present new advances in aging research and to stimulate collaborative research in this area. The symposium has grown over the past 10 years to be one of the biggest events at Harvard Medical School. We have been fortunate to have many of the leaders in the aging field speak 9:00 – 9:45 a.m. Introduction at the symposia and today is no exception. We wish to acknowledge the generosity and vision of Paul F. Glenn, Mark 9:45 – 10:15 a.m. Ensuring the Health of the Germ-line Collins and Leonard Judson for their unwavering support of aging research Cynthia Kenyon, Ph.D. through the Paul F. Glenn Foundation. Thanks to their support, we now have a vibrant community of researchers who study aging and age-related 10:15 – 10:45 a.m. C. elegans Surveillance of Core Cellular diseases. Since the inception of the Paul F. Glenn labs at Harvard in 2005, Components to Detect and Defend Pathogen this network has grown to include aging studies at the Albert Einstein Attacks, and How This Relates to Longevity College of Medicine, the Buck Institute, the Mayo Clinic, Massachusetts Gary Ruvkun, Ph.D.
    [Show full text]
  • The Journal of the Palo Alto Institute
    PAI is a 501(c)(3) nonprofit Vol. 5 creativity laboratory, The Journal of the dedicated to the pursuit February 2012 and promotion of unconventional truths ISSN: 1948–7843 through research, Palo Alto Institute education and entertainment. E-ISSN: 1948–7851 Future of Human Evolution 1 Status Update 13 Food Allergy, Asthma, Anaphylaxis, and Autonomic Dysfunction 17 10x 22 Therapeutics as the Next Frontier in the Evolution of Darwinian Medicine 24 Future of Human Evolution Palo Alto Institute Joon Yun February 2012, Vol. 5 DOI: 10.3907 / FHEJ5P Programmed Death Is senescence (biologic death) a programmed trait? Perhaps no topic in evolutionary biology evokes more controversy. Senescence was once assumed to be the result of so-called "wear and tear"; namely, an organism ages and eventually fails as it accumulates defects that are insufficiently corrected. However, the existence of senescence is not a thermodynamic necessity. Although entropy must increase within a closed system, organisms are not closed systems unto themselves. Since it can extract free energy from the environment and reduce its own entropy, an organism typically grows more resilient from seed stage to reproductive maturity. Indeed, life tables for humans suggest that the lowest likelihood of death in females occurs around the age of 14, which coincides with the prehistoric age of reproductive maturity. Organisms appear to be capable of self-repair when beneficial; indeed, certain organisms such as Hydra do not exhibit signs of senescence. However, most organisms undergo a failure of repair mechanisms, an increase in entropy, and an emergence of senescence after reproductive age—despite having free energy available around them.
    [Show full text]
  • Aging by Design
    Aging by Design How New Thinking on Aging Will Change Your Life Theodore C. Goldsmith Copyright © 2011 Azinet Press ISBN: 978-0-9788709-3-5 ISBN-10: 0-9788709-3-X Amazon Kindle Edition ASIN: B005KCO8SS Azinet Press Box 239 Crownsville, MD 21032 1-410-923-4745 Keywords: senescence, anti-aging medicine, ageing, evolution, gerontology This book contains some material previously published in An Introduction to Biological Aging Theory Pictures and illustrations courtesy of Wikipedia unless otherwise noted. 22,500 words, 49 pages (8.5 x 11 inch format), 7 illus. August 22, 2011 2 Contents Introduction......................................................................................................................... 4 Ages of Man – Human Mortality........................................................................................ 5 A Brief Summary of Aging Theories.................................................................................. 6 The Evolution of Aging ...................................................................................................... 7 Medawar’s Modification to Darwin’s Theory .................................................................. 11 Williams’ Modification to Darwin’s Theory .................................................................... 12 Evolution Theory’s Individual Benefit Clause ................................................................. 14 More Discrepancies with Traditional Darwinism – Group Selection............................... 15 More Discrepancies – Evolvability
    [Show full text]
  • David Sinclair Can Dramatically Extend the Life Span of Yeast
    News Focus Lenny Guarente and his former postdoc David Sinclair can dramatically extend the life span of yeast. They’re battling over how this works, and competing head-to-head to grant extra years to humans Aging Research’s Family Feud BOSTON AND CAMBRIDGE,MASSACHUSETTS—At tenure-track spot on Harvard’s faculty in late share many traits common among successful 34, David Sinclair is a rising star. His spa- 1999. He then made clear that his old profes- scientists. Both are deeply ambitious, relent- cious ninth-floor office at Harvard Medical sor’s pet theories weren’t off limits. At a lessly competitive, and supremely self-confi- School boasts a panoramic Boston view. His meeting at Cold Spring Harbor Laboratory dent. Both savor the limelight. Both love sci- rapidly growing lab pulled off the feat of pub- in late 2002, Sinclair surprised Guarente by ence and show little interest in other pursuits. lishing in both Nature and Science last year, challenging him on how a key gene Guarente Still, they’ve retained something of the and it made headlines around the world with discovered extends life in yeast. That sparked parent-child relationship that can shape in- a study of the possible antiaging properties of a bitter dispute that crescendoed this winter, teractions between senior researchers and a molecule found in red wine. In a typical when the pair published dueling papers. their students. Like a father dismayed when day, he fields calls from a couple practicing a Researchers who study aging are finding his son joins a punk rock band, and then dis- radical diet to extend life span, and from an the quarrel both intellectually provocative and mayed further when it attracts devoted fans actor hunting for antiaging pills and the a lively source of gossip.
    [Show full text]
  • An Age Dependent Mechanism of Mammals Self Destruction
    Ukrainica Bioorganica Acta 1—2 (2004) 3—12 www.bioorganica.org.ua Do mammals die young!? An agedependent mechanism of mammals selfdestruction O. G. Boyko MultiВranched Centre of Science & Technology «Agrobiotech» 50 Kharkivski highway, Kyiv, 02160, Ukraine Abstract. It is hypothesized the first multicellular organisms arisen on the Earth have inherited neither cell aging nor programmed cell death mechanisms from singlecellular ancestors possessing practically unlimited longevity. Both aging and aginginduced death are later evolutionary acquisitions. They are typical only for some phyla, and the majority of nowadays species of multicellular organisms are potentially immortal. Cell aging mechanisms in multicellular organisms can be somewhat involved in agedependent mechanisms of self destruction, but they cannot determine themselves the organism’s aging and longevity. An agerelated mecha nism of mammal selfdestruction appears in the evolutionary lineage from mammallike reptiles Synapsida to mammals in addition to existing systemic and cellular mechanisms of aging. Such agerelated mechanism direct ing the selfdestruction of mammal’s organism is a result of some evolutionary events leading to the «postmitot ic brain» development in mammals. In this minireview, recent results relevant to this hypothesis are surveyed and some approaches to intervening in the proposed process are discussed. Keywords: aging, hypothesis, mammals, birds, exogenous organospecific RNAs, postmitotic brain. Introduction. The ultimate aim of gerontology lachev’s version, potential immortality has alrea researches is to make human aging optional. dy considered not as a luxury, but as a fatal dan Therefore, the initial purpose of this work was ger for population, contrary to initial Weismann’s to consider the most important facts and ideas and conception.
    [Show full text]
  • Ageing Research Reviews Revamping the Evolutionary
    Ageing Research Reviews 55 (2019) 100947 Contents lists available at ScienceDirect Ageing Research Reviews journal homepage: www.elsevier.com/locate/arr Review Revamping the evolutionary theories of aging T ⁎ Adiv A. Johnsona, , Maxim N. Shokhirevb, Boris Shoshitaishvilic a Nikon Instruments, Melville, NY, United States b Razavi Newman Integrative Genomics and Bioinformatics Core, The Salk Institute for Biological Studies, La Jolla, CA, United States c Division of Literatures, Cultures, and Languages, Stanford University, Stanford, CA, United States ARTICLE INFO ABSTRACT Keywords: Radical lifespan disparities exist in the animal kingdom. While the ocean quahog can survive for half a mil- Evolution of aging lennium, the mayfly survives for less than 48 h. The evolutionary theories of aging seek to explain whysuchstark Mutation accumulation longevity differences exist and why a deleterious process like aging evolved. The classical mutation accumu- Antagonistic pleiotropy lation, antagonistic pleiotropy, and disposable soma theories predict that increased extrinsic mortality should Disposable soma select for the evolution of shorter lifespans and vice versa. Most experimental and comparative field studies Lifespan conform to this prediction. Indeed, animals with extreme longevity (e.g., Greenland shark, bowhead whale, giant Extrinsic mortality tortoise, vestimentiferan tubeworms) typically experience minimal predation. However, data from guppies, nematodes, and computational models show that increased extrinsic mortality can sometimes lead to longer evolved lifespans. The existence of theoretically immortal animals that experience extrinsic mortality – like planarian flatworms, panther worms, and hydra – further challenges classical assumptions. Octopuses pose another puzzle by exhibiting short lifespans and an uncanny intelligence, the latter of which is often associated with longevity and reduced extrinsic mortality.
    [Show full text]
  • Genes That Act Downstream of DAF-16 to Influence the Lifespan Of
    articles Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans Coleen T. Murphy*, Steven A. McCarroll†, Cornelia I. Bargmann†, Andrew Fraser‡, Ravi S. Kamath‡, Julie Ahringer‡, Hao Li* & Cynthia Kenyon* * Department of Biochemistry and Biophysics, and † Department of Anatomy and Howard Hughes Medical Institute, University of California, San Francisco, California 94143-2200, USA ‡ Wellcome CRC Institute and Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK ........................................................................................................................................................................................................................... Ageing is a fundamental, unsolved mystery in biology. DAF-16, a FOXO-family transcription factor, influences the rate of ageing of Caenorhabditis elegans in response to insulin/insulin-like growth factor 1 (IGF-I) signalling. Using DNA microarray analysis, we have found that DAF-16 affects expression of a set of genes during early adulthood, the time at which this pathway is known to control ageing. Here we find that many of these genes influence the ageing process. The insulin/IGF-I pathway functions cell non- autonomously to regulate lifespan, and our findings suggest that it signals other cells, at least in part, by feedback regulation of an insulin/IGF-I homologue. Furthermore, our findings suggest that the insulin/IGF-I pathway ultimately exerts its effect on lifespan by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes. The recent discovery that the ageing process is regulated hormonally never been tested directly; for example, by asking whether stress by an evolutionarily conserved insulin/IGF-I signalling pathway1–3 response genes are required for the longevity of daf-2 mutants.
    [Show full text]
  • From Here to Immortality: Anti-Aging Medicine
    FromFrom HereHere toto Immortality:Immortaalitty: AAnti-AgingAnnntti-AAgging MMedicineedicine Anti-aging medicine is a $5 billion industry. Despite its critics, researchers are discovering that inter ventions designed to turn back time may prove to be more science than fiction. By Trudie Mitschang 14 BioSupply Trends Quarterly • October 2013 he symptoms are disturbing. Weight gain, muscle Shifting Attitudes Fuel a Booming Industry aches, fatigue and joint stiffness. Some experience The notion that aging requires treatment is based on a belief Thear ing loss and diminished eyesight. In time, both that becoming old is both undesirable and unattractive. In the memory and libido will lapse, while sagging skin and inconti - last several decades, aging has become synonymous with nence may also become problematic. It is a malady that begins dete rioration, while youth is increasingly revered and in one’s late 40 s, and currently 100 percent of baby boomers admired. Anti-aging medicine is a relatively new but thriving suffer from it. No one is immune and left untreated ; it always field driven by a baby- boomer generation fighting to preserve leads to death. A frightening new disease, virus or plague? No , its “forever young” façade. According to the market research it’s simply a fact of life , and it’s called aging. firm Global Industry Analysts, the boomer-fueled consumer The mythical fountain of youth has long been the subject of base will push the U.S. market for anti-aging products from folklore, and although it is both natural and inevitable, human about $80 billion now to more than $114 billion by 2015.
    [Show full text]
  • Alchemy of Aging
    BOOK REVIEW Alchemy of aging The twists and turns of the discovery of telomerase, the cloning of the gene and the demonstration of its immortalizing Merchants of Immortality: Chasing power in cell culture systems are well told. Along the way, we the Dream of Human Life Extension learn of the squabbles, too. A sad axiom of modern biology, reflects Hall, is that the hotter the field, the ruder the behavior of Stephen S Hall its practitioners. Sad, perhaps, but as Hall very well knows, it Houghton Mifflin Company, 2003 makes for good copy. Although Hall documents his sources exhaustively, in more than 439 pp. hardcover, $25.00 50 pages of notes, his scientific range is limited. For example, he ISBN 0-61809-524-1 does not do as much as is needed to put the telomerase work into context. As the field has advanced, it has emerged that there is much Reviewed by Tom B L Kirkwood more to controlling cell proliferation than telomerase and that there is much more to tissue aging than just the Hayflick Limit. Unquestionably, the work included in Hall’s account is of great sig- nificance. But when and how it might lead to any real prospect of http://www.nature.com/naturemedicine For a work of engaging and painstaking science journalism, one intervention to extend human lifespan is anybody’s guess. Some of would have to search far to find anything that beats Stephen S. Hall’s the most interesting research in the field of aging is being done on Merchants of Immortality.This is the good news.
    [Show full text]
  • Clark2019.Pdf (4.792Mb)
    This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. Model Organisms to Models: How Ageing Affects Infectious Disease Dynamics Jessica Clark A thesis submitted for the degree of Doctor of Philosophy The University of Edinburgh 2019 Declaration I declare that this thesis has been composed by myself and that the work has not been submitted for any other degree or professional qualification. I confirm that the work submitted is my own, except where work which has formed part of jointly-authored publications has been included. My contribution and those of the other authors to this work have been explicitly indicated below. I confirm that appropriate credit has been given within this thesis where reference has been made to the work of others. The work presented in Chapter 2 was previously published in Ecology Letters as Disease Spread in Age Structured Populations with Maternal Age Effects by Jessica Clark (Author of Declaration & Student), Jenny Garbutt (Research Group Member), Luke McNally (Collaborator) & Tom Little (Primary Supervisor).
    [Show full text]
  • Real-Time Egg Laying Dynamics in Caenorhabditis Elegans
    UNIVERSITY OF CALIFORNIA, IRVINE Real-time egg laying dynamics in Caenorhabditis elegans DISSERTATION submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Biomedical Engineering by Philip Vijay Thomas Dissertation Committee: Professor Elliot Hui, Chair Professor Olivier Cinquin Professor Abraham Lee 2015 c 2015 Philip Vijay Thomas TABLE OF CONTENTS Page LIST OF FIGURES iv ACKNOWLEDGMENTS v CURRICULUM VITAE vi ABSTRACT OF THE DISSERTATION viii 1 Introduction and motivation 1 1.1 The impact of C. elegans in aging and lifespan studies along with current limitations . 1 1.2 Starvation and its effect on worms . 4 1.3 Microfabricated systems for C. elegans biology . 5 2 Real-time C. elegans embryo cytometry to study reproductive aging 7 2.1 High capacity low-weight passive bubble trap . 8 2.2 Microfluidic device layout . 10 2.3 Tuning habitat exit sizes to flush out embryos while retaining worms . 11 2.4 Equal flow resistance to make identical habitats . 12 2.5 Video enumeration of eggs . 13 2.6 Switching between discrete and continuously varying media concentrations . 15 3 Optimizing worm health in C. elegans microfluidics 17 3.1 E. coli densities of 1010 cells/mL maintain egg-laying in liquid worm culture 18 3.2 E. coli biofilms in devices . 19 3.3 Amino acid addition to S-media, γ irradiation of bacteria, and elevated syringe temperatures are ineffective in reducing biofilms in devices . 20 3.4 Use of a curli major subunit deletion strain significantly reduces biofilm in S-media . 23 4 Conclusions and future directions 26 Bibliography 30 ii A Appendix Title 41 A.1 Methods .
    [Show full text]
  • ER Galimov1, JN Lohr1, and D. Gems1,A
    MINI-REVIEW When and How Can Death Be an Adaptation? E. R. Galimov1, J. N. Lohr1, and D. Gems1,a* 1Institute of Healthy Ageing, Research Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK ae-mail: [email protected] * To whom correspondence should be addressed. Abstract—The concept of phenoptosis (or programmed organismal death) is problematic with respect to most species (including humans) since it implies that dying of old age is an adaptation, which contradicts the established evolutionary theory. But can dying ever be a strategy to promote fitness? Given recent developments in our understanding of the evolution of altruism, particularly kin and multilevel selection theories, it is timely to revisit the possible existence of adaptive death. Here, we discuss how programmed death could be an adaptive trait under certain conditions found in organisms capable of clonal colonial existence, such as the budding yeast Saccharomyces cerevisiae and, perhaps, the nematode Caenorhabditis elegans. The concept of phenoptosis is only tenable if consistent with the evolutionary theory; this accepted, phenoptosis may only occur under special conditions that do not apply to most animal groups (including mammals). DOI: 10.1134/S000629791912001? Keywords: adaptive death, aging, altruism, C. elegans, evolution, inclusive fitness PROGRAMMED AGING AND PHENOPTOSIS Is aging programmed? Asking this question risks falling afoul of the old warning: ask a stupid question and you’ll get a stupid answer [1, 2]. This is because the term programmed aging has multiple meanings, which can lead the questioner into logical confusion [3]. But it is possible to disambiguate this term and to avoid conceptual pratfalls, as follows.
    [Show full text]