Aging of Organisms PDF
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AGING OF ORGANISMS BIOLOGY OF AGING AND ITS MODULATION VOLUME4 AGING OF ORGANISMS Edited by HEINZ D. OSIEWACZ J W Goethe University Frankfurt Germany SPRINGER-SCIENCE+BUSINESS MEDIA, B.V. Library of Congress Cataloging-in-Publication Data is available. ISBN 978-90-481-6332-8 ISBN 978-94-017-0671-1 (eBook) DOI 10.1007/978-94-017-0671-1 Printed on acid-free paper All Rights Reserved © 2003 Springer Science+Business Media Dordrecht Originally published by Kluwer Academic Publishers in 2003 Softcover reprint of the hardcover 1st edition 2003 No part of this publication may be reproduced or utilized in any form or by any means, electronic, mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the copyright owner. Contents Editorial: About the series "Biology of aging and its modulation" S. Rattan vn Preface Heinz D. Osiewacz IX Chapter 1. Yeast longevity and aging S. Michal Jazwinski Chapter 2. Aging and longevity in the filamentous fungus Podosporo anserina Heinz D. Osiewacz 31 Chapter 3. Genetic, metabolic and environmental factors associated with aging in plants Karin Krupinska, Jon Falk and Klaus Humbeck 55 Chapter 4. Aging in sponges Heinz C. Schroder, Matthias Wiens and Werner E. G. Muller 79 Chapter 5. Aging and environmental conditions in insects Klaus-GUnter Collatz 99 Chapter 6. Genetics of aging in Drosophila Linda Partridge and Scott D. Pletcher 125 Chapter 7. Aging in C. elegans Anders Olsen, James N Sampayo and Gordon J. Lithgow 163 Chapter 8. Aging in birds Donna J. Holmes 201 Chapter 9. Exploring the mechanism of aging using rodent models Yuji !keno and Holly Van Remmen 221 Chapter 10. Human aging and longevity: genetic aspects Holger Hoehn and Armin Renner 247 Index 271 About the series "Biology of aging and its modulation" During the last 40 years, the study of the biological basis of aging has progressed tremendously, and it has now become an independent and respectable field of study and research. Several universities, medical institutes and research centers throughout the world now offer full-fledged courses on biogerontology. The interest of students taking such courses, followed by undertaking research projects for MSc and PhD studies, has also increased significantly. Cosmetic, cosmeceutical and pharmaceutical industry's ever increasing interest in aging research and therapy is also obvious. Moreover, increased financial support by the national and international financial agencies to biogerontological research has given much impetus to its further development. This five-volume series titled "Biology of Aging and its Modulation" fulfills the demand for books on the biology of aging, which can provide critical and comprehensive overview of the wide range of topics, including the descriptive, conceptual and interventive aspects of biogerontology. The titles of the books in this series and the names of their respective editors are: 1. Aging at the molecular level (Thomas von Zglinicki, UK) 2. Aging of cells in and outside the body (S. Kaul and R. Wadhwa, Japan) 3. Aging of organs and systems (R. Aspinall, UK) 4. Aging of organisms (H. D. Osiewacz, Germany) 5. Modulating aging and longevity (S. Rattan, Denmark) The target readership is both the undergraduate and graduate students in the universities, medical and nursing colleges, and the post-graduates taking up research projects on different aspects of biogerontology. We hope that these books will be an important series for the college, university and state libraries maintaining a good database in biology, medical and biomedical sciences. Furthermore, these books will also be of much interest to pharmaceutical, cosmaceutical, nutraceutical and health care industry for an easy access to accurate and reliable information in the field of aging research and intervention. Suresh IS. Rattan, Ph.D., D.Sc. Series Editor and Editor-in-Chief, Biogerontology Danish Centre for Molecular Gerontology, Department of Molecular Biology, University of Aarhus, Denmark Preface Biological aging as the time-depending general decline of biological systems associated with a progressively increasing mortality risk is a general phenomenom of great significance. The underlying processes are very complex and depending on genetic and environment factors. These factors encode or affect a network of interconnected cellular pathways. In no system this network has been deciphered in greater detail. However, the strategy of studying various biological systems has let to the identification of pathways and specific modules and makes it obvious that aging is the result of different overlapping mechanisms and pathways. Some of these appear to be conserved ("public") among species, others are specific or "private" and only of significance in one or a few organisms. This volume in the series on "Biology of aging and its modulation" specifically focuses on organismic aging. The book covers research on organisms from lower to higher complexity representing examples from very diverse taxa like photosynthetic plants, fungi, sponges, nematodes, flies, birds and mammals. Such a broad treatise of this complex topic provides a comprehensive "flavor" about the current issues dealt with in this rapidly growing scientific discipline. Heinz D. Osiewacz Frankfurt, Juli 2003 Yeast Longevity and Aging S. Michal Jazwinski Department of Biochemistry and Molecular Biology, LSU Health Sciences Center, 1901 Perdido Street, New Orleans, LA 70112, USA Definitions of yeast aging The possibility that the yeast Saccharomyces cerevisiae may be prone to age changes in its reproductive potential was first pointed out by Barton [1]. This suggestion was based on the observation that cell division is associated with the deposition of a "bud scar" on the surface of the mother cell. This fundamental aspect of reproduction was subsequently affirmed and expanded upon [2-4], and its cumulative features were directly demonstrated [5]. The finite budding or reproductive/replicative capacity of individual yeast cells was clearly shown by Mortimer and Johnston [6]. These authors reasoned that non disjunction or recessive lethal genetic changes, other deleterious nuclear events or random depletion of essential autonomous cytoplasmic constituents are not likely to explain the finite replicative life span, because the original population is already at equilibrium for such events. This led to the conclusion that genetic mutation theories are not likely to explain the limitations on yeast life span [7]. However, this rationale does not encompass the cumulative effects of damage and functional losses within individual yeast cells as they progress through their replicative life spans. Progeny cells may be shielded from such damage, which may make its presence known primarily in parental cells. If excessive, functional losses of this sort would be selected against in the population. In any event, they would not impact the fitness of the population as explained later. A life span limited by the number of divisions available to the cell has recently been demonstrated in the fission yeast Schizosaccharomyces pombe [8]. This discovery required a cunning analysis of the development of age asymmetry in lineages of cells dividing by fission. Thus far, this experimental system has not been exploited. We will not refer to this yeast any further in this article. HD. Osiewacz (ed.), Aging of Organisms, 1-30. © 2003 Kluwer Academic Publishers. 2 S. MICHAL JAZWINSKI Yeasts gradually lose viability when they are maintained in stationary phase [9]. Under these conditions of nutrient depletion, the cells exhibit markedly reduced metabolic activity compared to exponentially growing cells [9, 10]. However, metabolic time is still running [1 1, 12], and it can clearly impact the subsequent replicative life span of the cells [12, 13]. The loss of viability in stationary phase is used to define the chronological life span of yeast cells [14]. Dividing yeast cells display an exponential increase in mortality rate with age [15, 16]. The mortality rate, however, plateaus for the last ten percent or so of an aging cohort [17]. On the other hand, mortality rate fluctuates wildly during the yeast chronological life span, exhibiting increases, decreases and plateaus [18]. Phenomenology of yeast aging During the quarter of a century following the discovery of the limited replicative capacity of yeast cells, most of the attention was focused on a description of the changes that occur in these cells as they progress through their life spans. Some of these studies were ingenious in employing manipulations of these cells to provide insights into the mechanisms underlying this phenomenon. The laboratory of Ilse Muller played the leading role during this period. Of utmost significance was the finding that the number of divisions available to yeast cells was not altered by holding them in a non-dividing state through nutrient elimination [19]. The cells essentially picked up where they left off in completing their remaining life spans. There is no discrepancy between this finding and the loss of viability or curtailment oflife span of cells held in stationary phase, mentioned earlier, because the issue in this case is related to the number of cell divisions remaining for completion of the life span and not those available to cells held in stationary phase to begin with. Since Johnston [20] determined that daughter cells have the same life span as their mothers had, it has been assumed that cell division involves the establishment of age asymmetry between mother and daughter. In other words, regardless of the nature of the "clock" measuring life span, it is reset in the daughter. Indeed, this principle is maintained throughout the bulk of the life span [11]. However, it breaks down for daughter cells produced from mothers late in their life spans [A. Rogel and I. MUller cited in ref. 11]. Daughters of old cells have a shorter life span than daughters of young cells. This finding has been affirmed [21]. Owing to the limited number of cells examined, Johnston [20] would not have recognized this fate of daughters of old mothers. Johnston [20] also determined that cells that cease dividing early in the life span of the cohort frequently fail to release their daughters in a viable form, while cells displaying longer life spans do this rarely. This suggests that it may be possible to distinguish a phenomenon of premature death. However, such premature demise may be peculiar to the particular yeast strain. Recently, McVey et al. [22] have confirmed the finding that normal yeasts cease dividing as unbudded cells [23]. They also showed that certain mutations that shorten life span lead to two distinct populations of cells. The first ceases division as large-budded cells and has short life spans, while the second arrests as unbudded cells and has longer life spans. These
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