[Paleopsych] SW: Mortality and Lifespan

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Evolutionary Biology: Mortality and Lifespan
http://scienceweek.com/2004/sc041217-1.htm

    The following points are made by Peter A. Abrams (Nature 2004
    431:1048):
    1) Recent work(1) has involved an investigation of one of the main
    factors that influence the evolution of an organism's lifespan. That
    factor is the risk of dying that a population faces as a result of
    environmental conditions (e.g., predation). The study subjects were
    guppies, small tropical fish that are widely used in evolutionary
    studies, and the authors have provided the first experimental support
    for the prediction that a higher environmental risk of mortality can
    select for inherently longer-lived organisms.
    2) Guppies from the lower reaches of several rivers in Trinidad are
    subject to much higher rates of predation than those in the upper
    parts of the same rivers, where waterfalls block access by larger
    fish. In predator-free lab experiments, Reznick et al(1) found that
    guppies from the high-predation segments of two of the rivers lived up
    to 35% longer than those from low-predation segments of the same
    watercourse. In addition, the guppies from high-predation sites had a
    40% longer reproductive span and reproduced at a higher rate. So a
    background of higher mortality under natural conditions has apparently
    led to the evolution of both a longer lifespan and a longer
    reproductive span.
    3) Some history is required to see why this observation is surprising.
    Environmentally caused ("extrinsic") mortality has long been
    recognized as a key factor determining how natural selection molds
    "intrinsic" mortality -- the death rate that a population would have
    under some standardized, generally benign, set of environmental
    conditions. Although evolution should favor lower intrinsic mortality
    (and a longer intrinsic lifespan) when all else is equal, many
    organisms face a trade-off between higher levels of reproduction or
    lower levels of intrinsic mortality. One of the main reasons that
    senescence occurs is because repair is costly: resources that are
    devoted to maintaining an organism are not available for reproduction.
    In the 1950s, Peter Medawar(2) and George Williams(3) pointed out that
    high extrinsic mortality could favor shorter intrinsic lifespan. Why,
    they reasoned, should an organism invest in costly repair that will
    probably only ensure that it is in prime physical condition when its
    life ends? Higher extrinsic mortality should favor low investment in
    repair, and thus a high intrinsic mortality and a short intrinsic
    lifespan.
    4) But this reasoning did not take account of two further factors. One
    is that higher extrinsic mortality also slows the rate of population
    growth, and more slowly growing populations are expected to evolve to
    have lower rates of intrinsic mortality and a longer lifespan(4,5).
    The other factor is the interaction between extrinsic mortality
    factors and physiological repair or maintenance(5). If predators can
    be evaded by fast, but not by slow prey, greater predation risk should
    select for greater maintenance of the body systems essential for fast
    movement. This higher level of repair would then prolong intrinsic
    lifespan.
    References (abridged):
    1. Reznick, D. N., Bryant, M. J., Roff, D., Ghalambor, C. K. &
    Ghalambor, D. E. Nature 431, 1095-1099 (2004)
    2. Medawar, P. B. An unsolved problem in Biology (Lewis, London)
    3. Williams, G. C. Evolution 11, 398-411 (1957)
    4. Charlesworth, B. A. Evolution in Age-Structured Populations
    (Cambridge Univ. Press, 1980)
    5. Abrams, P. A. Evolution 47, 877-887 (1993)
    Nature http://www.nature.com/nature
    --------------------------------
    Related Material:
    SIGNALS FROM THE REPRODUCTIVE SYSTEM REGULATE THE LIFESPAN OF C.
    ELEGANS.
    The following points are made by H. Hsin and C. Kenyon (Nature 1999
    399:308):
    1) Understanding how the ageing process is regulated is a fascinating
    and fundamental problem in biology. The authors demonstrate that
    signals from the reproductive system influence the lifespan of the
    nematode Caenorhabditis elegans. If the cells that give rise to the
    germ line are killed with a laser microbeam, the lifespan of the
    animal is extended.
    2) The authors suggest their findings indicate that germline signals
    act by modulating the activity of an insulin/IGF-1 (insulin-like
    growth factor) pathway that is known to regulate the ageing of this
    organism. Mutants with reduced activity of the insulin/IGF-1-receptor
    homologue DAF-2 have been shown to live twice as long as normal, and
    their longevity requires the activity of DAF- 16, a member of the
    forkhead/winged-helix family of transcriptional regulators.
    3) The authors find that in order for germline ablation to extend
    lifespan, DAF-16 is required, as well as a putative nuclear hormone
    receptor, DAF-12. In addition, the findings suggest that signals from
    the somatic gonad also influence ageing, and that this effect requires
    DAF-2 activity.
    4) The authors suggest that together their findings imply that the C.
    elegans insulin/IGF-1 system integrates multiple signals to define the
    animal's rate of ageing. The authors suggest this study demonstrates
    an inherent relationship between the reproductive state of this animal
    and its lifespan, and may have implications for the co-evolution of
    reproductive capability and longevity.
    Nature http://www.nature.com/nature
    --------------------------------
    Related Material:
    AGING, LIFESPAN, AND SENESCENCE
    Notes by ScienceWeek:
    Our knowledge of the basis of senescence of cells, tissues, and
    organisms (including humans) has entered a new phase in recent decades
    because of the new vistas opened by molecular biology. Model systems
    have started to provide insights, and one important approach has been
    the identification of genes that determine the lifespan of an
    organism. The very existence of genes that when mutated can extend
    lifespan suggests to many researchers that one or a few processes may
    be critical in aging, and that a slowing of these processes may slow
    aging itself.
    The following points are made by L. Guarente et al (Proc. Nat. Acad.
    Sci. 1998 95:11034):
    1) In the budding yeast Saccharomyces cerevisiae, aging results from
    the asymmetry of cell division, which produces a large mother cell and
    a small daughter cell arising from the bud. Much of the macromolecular
    composition of the daughter cell is newly synthesized, whereas the
    composition of the mother cell grows older with each cell division. It
    has been shown that mother cells of this yeast species divide a
    relatively fixed number of times, and exhibit a slowing of the cell
    cycle, cell enlargement, and sterility. Analysis of *ribosomal DNA in
    old cells reveals an accumulation of *extrachromosomal ribosomal DNA
    of discrete sizes, apparently representing a cumulative fragmentation
    of chromosomal ribosomal DNA. The authors suggest it will be of great
    interest to assess the generality of this process as an aging
    mechanism.
    2) In Caenorhabditis elegans, the *neurosecretory system regulates
    whether animals enter the reproductive life cycle or arrest
    development at a primitive *diapause stage. Developmental arrest is
    apparently induced by a *pheromone and involves behavioral and
    morphological changes in many tissues of the animal, with the lifespan
    becoming 4 to 8 times longer than that of the normal 3-week lifespan
    of fully developed animals. Declines in pheromone concentration induce
    recovery to reproductive adults with normal metabolism and lifespan.
    Genes that regulate the function of the C. elegans diapause and the
    neuroendocrine aging pathway have been identified, and at least one of
    these genes codes for an *insulin-like receptor apparently involved in
    metabolism. The authors suggest that if the association of longevity
    and diapause is general, it is possible that *polymorphisms in the
    human insulin receptor-signaling pathway genes and related gene
    *homologues may underlie genetic variation in human longevity.
    3) In plants, there is a large range of lifespans in the various plant
    kingdoms. Certain tree species live for well over a century, whereas
    other plants complete their life cycle in a few weeks. The "yellowing"
    of leaves is often referred to in the plant literature as leaf
    senescence or the "senescence syndrome" -- referring to the process by
    which nutrients are mobilized from the dying leaf to other parts of
    the plant to support their growth. The senescence syndrome is
    characterized by distinct cellular and molecular changes, with the
    chloroplast the first part of the cell to undergo disassembly
    (producing the "yellowing"). In many plant species, certain hormones
    can either enhance or delay senescence. Although the genes that are
    expressed during the plant senescence syndrome (as well as ways to
    manipulate such senescence) have been identified, much remains to be
    done to understand the molecular basis of aging in plants. For
    example, nothing is known about the signal transduction pathways that
    lead to altered gene expression during senescence, or how plant
    hormones such as *cytokinin influence senescence. But there are now
    many tools to explore this process. The authors conclude: "It remains
    to be seen whether common mechanisms link the aging process in diverse
    organisms."
    Proc. Nat. Acad. Sci. http://www.pnas.org
    --------------------------------
    Notes by ScienceWeek:
    ribosomal DNA: A ribosome (not to be confused with riboZYME) is a
    small particle, a complex of various ribonucleic acid component
    subunits and proteins that functions as the site of protein synthesis.
    The term "ribosomal DNA" refers to the gene or genes that code for the
    RNA in ribosomes. In other words, the term "ribosomal DNA" does not
    refer to any DNA in ribosomes (there is no DNA in ribosomes).
    extrachromosomal: In general, this refers to anything outside of
    chromosomes, and in this case to DNA fragments unincorporated into
    chromosomal DNA.
    neurosecretory system: In general, all neural systems contain both
    neurons that themselves secrete chemical messengers and neurons that
    signal special secretory cells to secrete chemical messengers. A
    neurosecretory pathway is a delineated signaling system that involves
    such a resultant secretion.
    diapause: In general, this refers to any programmed period of
    suspended development in invertebrates.
    pheromone: In general, a chemical substance which, when released into
    an animal's surroundings, influences the development or behavior of
    other individuals of the same species.
    insulin: A protein hormone that promotes uptake by body cells of free
    glucose and/or amino acids, depending on target cell type.
    polymorphisms: A genetic polymorphism is a naturally occurring
    variation in the normal nucleotide sequence of the genome within
    individuals in a population. Variations are denoted as polymorphisms
    only if they cannot be accounted for by recurrent mutation and occur
    with a frequency of at least about 1 percent.
    homologues: In general, the term "homologous" means having the same
    structure. But the term has special uses in genetics and evolution
    biology.
    cytokinin: A group of plant growth substances. They are chemically
    identified as derivatives of the purine base adenine. They stimulate
    cell division and determine the course of differentiation. They work
    synergistically with other plant hormones called "auxins".