Table Of ContentAGING 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
